Technical articles
CTLA4 Signaling Pathway: Molecular Basis, Immunoregulatory Mechanisms, and Disease Associations
CTLA4 Signaling Pathway: Molecular Basis, Immunoregulatory Mechanisms, and Disease Associations
CTLA4 is a key negative regulatory molecule within the T-cell costimulatory network and participates in setting the threshold for initial activation, limiting clonal expansion, mediating Treg-dependent immunosuppression, and maintaining peripheral tolerance. Analysis of the CTLA4 pathway should be placed within an integrated framework that includes the CD28 costimulatory axis, ligand availability on antigen-presenting cells, receptor intracellular trafficking, and regulation by the immune microenvironment.
Keywords: CTLA4; CD28; CD80; CD86; T-cell costimulation; immune checkpoint; Treg; immune tolerance
1 Basic Functional Positioning of the CTLA4 Signaling Pathway
1.1 Functional Position Within the Costimulatory Network
(1) Dual-signal basis of T-cell activation
Initial T-cell activation generally requires the coordinated integration of two classes of signals. Signal 1 is delivered through TCR recognition of the peptide-MHC complex and determines antigen specificity; Signal 2 is mediated primarily by CD28 and determines whether T cells enter a state of full proliferation and effector differentiation. When costimulation is insufficient, even if the TCR has been engaged, T cells may enter a state of hyporesponsiveness, anergy, or tolerance-associated dysfunction.
(2) Negative regulatory role within the costimulatory axis
CTLA4 shares CD80 and CD86 as ligands with CD28, but the two receptors exert opposing functions. CD28 promotes IL-2 production, cell-cycle progression, and effector expansion, whereas CTLA4 constrains costimulatory intensity, raises the activation threshold, and suppresses excessive expansion. Accordingly, CTLA4 is not an isolated inhibitory molecule, but a balancing node within the costimulatory axis.
(3) Regulatory properties during the immune priming phase
Compared with certain inhibitory receptors that act more prominently during peripheral tissue effector phases, CTLA4 participates more deeply in the initial activation stage within lymphoid organs, particularly by influencing the degree of costimulation acquired by T cells at the surface of antigen-presenting cells. CTLA4 therefore exerts a marked effect on whether T cells undergo full priming.
1.2 Overall Logic of Pathway Function
(1) Competitive regulation of ligand availability
A central functional basis of CTLA4 lies in its competitive binding to CD80 and CD86. By reducing the probability that CD28 gains access to these ligands, CTLA4 attenuates costimulatory input, thereby restricting T-cell expansion and effector differentiation.
(2) Dual-level intracellular and extracellular regulation
The CTLA4 pathway includes both suppression of activation signaling within T cells and outward regulation of the availability of costimulatory molecules on antigen-presenting cells. It therefore affects not only the receptor-bearing cell itself but also indirectly shapes the priming conditions of surrounding T cells.
(3) Importance of Treg-dependent suppression
In conventional activated T cells, CTLA4 is typically induced after activation, whereas in regulatory T cells it is maintained at relatively high and sustained functional levels. Treg cells rely on CTLA4 to weaken the costimulatory capacity of antigen-presenting cells, making this mechanism a major component of CTLA4-mediated immunosuppression.
2 Molecular Structure and Expression Regulation of CTLA4
2.1 Structural Features
(1) Basic structural organization
CTLA4 is a member of the immunoglobulin superfamily and contains an extracellular ligand-binding domain, a transmembrane region, and a relatively short cytoplasmic tail. The extracellular domain mediates recognition of CD80 and CD86, the transmembrane region determines membrane localization, and the cytoplasmic tail participates in intracellular signaling regulation and receptor trafficking through short functional motifs.
(2) Signaling properties of the cytoplasmic tail
The CTLA4 cytoplasmic tail does not possess intrinsic tyrosine kinase activity. Its signaling function depends primarily on interactions with intracellular adaptor proteins, trafficking machinery, and phosphatase networks. Thus, the inhibitory effects of CTLA4 are manifested more through remodeling of signaling complexes and attenuation of costimulation than through classical receptor-catalyzed enzymatic activity.
(3) Dynamic nature of surface expression
A substantial proportion of CTLA4 resides in intracellular vesicular compartments, and its surface expression is governed by the balance among continuous endocytosis, recycling, and degradation. For this reason, CTLA4 function depends not only on total expression level but also strongly on its surface availability and membrane residence time.
2.2 Expression Profile Characteristics
(1) Basal state in resting T cells
Surface CTLA4 levels are generally low in resting naïve T cells, indicating that it is not primarily a constitutive inhibitory molecule before activation, but rather a feedback regulator progressively introduced during activation.
(2) Inducible expression in activated T cells
TCR and CD28 signaling can induce CTLA4 transcription and expand intracellular CTLA4 stores. As activation proceeds, CTLA4 is progressively upregulated and incorporated into a negative feedback circuit that restrains abnormal expansion driven by sustained high-intensity stimulation.
(3) Sustained expression in Treg cells
Within the Foxp3-regulated context, Treg cells usually maintain high CTLA4 expression, enabling long-term participation in antigen-presenting cell remodeling and peripheral immunosuppression.
2.3 Receptor Trafficking and Functional Stability
(1) Rapid endocytosis
CTLA4 exhibits a short surface residence time and is readily internalized. Therefore, the surface expression measured in a single flow cytometric analysis does not always fully reflect its intracellular reserve or overall regulatory capacity.
(2) Recycling process
Intracellular CTLA4 can be recycled back to the cell surface. If this process is impaired, functional surface expression may decline substantially even when total protein expression remains relatively preserved.
(3) Pathological significance of trafficking abnormalities
CTLA4 insufficiency may arise not only from defects in gene expression but also from abnormalities in intracellular trafficking, recycling, or membrane localization. The integrity of the CTLA4 pathway is therefore not merely an issue of expression, but also one of cellular localization and trafficking biology.
3 Ligand Competition Mechanism Between CTLA4 and CD28
3.1 Shared Ligand Platform
(1) Origin of CD80 and CD86
CD80 and CD86 are primarily expressed on the surface of antigen-presenting cells such as dendritic cells, B cells, and activated macrophages, forming the key ligand platform through which naïve T cells acquire costimulatory signals.
(2) Functional divergence of different receptors sharing the same ligands
Binding of CD28 to CD80 and CD86 promotes T-cell activation, whereas binding of CTLA4 to the same ligands constrains costimulatory input. Therefore, the distribution of a shared ligand between these two receptors directly influences the direction of the immune response.
3.2 Competitive Advantage for Ligand Binding
(1) Binding advantage
CTLA4 has a functional binding advantage over CD28 for both CD80 and CD86. Once CTLA4 expression increases, it can occupy costimulatory ligands more effectively and reduce CD28 signaling input.
(2) Amplification of competitive effects
The function of CTLA4 is not limited to local ligand occupancy. Because it can substantially alter ligand availability on antigen-presenting cells, its inhibitory effects can be amplified into a broader reduction in costimulation for multiple neighboring T cells.
3.3 Ligand Removal and Trans-cellular Regulation
(1) Trans-endocytosis
CTLA4 can mediate trans-endocytosis of CD80 and CD86 from the surface of antigen-presenting cells, followed by internalization and degradation, thereby reducing the density of costimulatory molecules on APCs.
(2) APC functional remodeling
When costimulatory molecules are persistently depleted from the APC surface, the capacity of APCs to support naïve T-cell activation declines, and the local immune microenvironment correspondingly shifts toward a suppressive state.
(3) Prominent role in Treg cells
Through high-level CTLA4 expression, Treg cells continuously reduce the surface abundance of CD80 and CD86 on APCs. This process is one of the major mechanisms by which Treg cells suppress effector T-cell activation.
Table 1. Functional Comparison Between CTLA4 and CD28
Comparative Dimension | CD28 | CTLA4 |
Ligands | CD80/CD86 | CD80/CD86 |
Primary functional direction | Costimulation, promotion of activation | Negative regulation, limitation of activation |
Main expression pattern | Constitutively expressed on naïve T cells | Induced after activation; highly expressed in Treg cells |
Effect on T-cell proliferation | Promotes IL-2 production and clonal expansion | Suppresses IL-2 production and clonal expansion |
Effect on APC ligand availability | Relatively limited ligand consumption | Markedly reduces CD80/CD86 availability |
Immunological consequence | Enhances initial activation | Raises activation threshold and maintains tolerance |
4 Inhibitory Mechanisms of the CTLA4 Signaling Pathway
4.1 Extracellular Regulatory Mechanisms
(1) Competitive suppression of costimulation
This is one of the core inhibitory mechanisms of CTLA4. By competing for CD80 and CD86, CTLA4 reduces CD28 signaling input and thereby suppresses IL-2 production, cell-cycle progression, and clonal expansion.
(2) Ligand removal mechanism
CTLA4 can remove CD80 and CD86 from the immunological synapse on APCs and promote their degradation, resulting in an overall reduction of costimulatory resources. This mechanism extends CTLA4-mediated inhibition beyond a single T cell and converts it into systemic regulation of the local immune microenvironment.
(3) Regulation of APC state
In certain settings, CTLA4 interactions with APCs can drive them toward a lower-costimulation state. This effect is strongly context-dependent, but it is important for the maintenance of tolerance and Treg-mediated suppression.
4.2 Intracellular Signal Inhibition Mechanisms
(1) Suppression of the CD28-PI3K-AKT axis
CTLA4 signaling is often accompanied by attenuation of the downstream CD28-PI3K-AKT-mTOR axis, leading to restricted metabolic reprogramming, reduced growth signaling, and diminished proliferative capacity.
(2) Repression of IL-2 transcription
CTLA4 can suppress activation-associated transcriptional programs and reduce IL-2 production. In naïve T cells, this means weakened proliferative drive; in effector T cells, it limits the ability to sustain ongoing responses.
(3) Reduced immunological synapse stability
CTLA4 can weaken or shorten the maintenance of stable immunological synapses primarily supported by TCR and CD28 signaling, thereby reducing the efficiency of cumulative activation signaling. The result is not complete blockade of antigen recognition, but a reduction in the persistence and strength of activation.
(4) Association with phosphatase networks
In multiple experimental systems, the CTLA4 cytoplasmic tail has shown functional association with regulatory molecules such as PP2A and SHP-2, and these interactions may contribute to downstream inhibitory effects. However, the relative contribution of direct intracellular inhibitory mechanisms is not fully consistent across models.
4.3 Functional Outcomes of the Pathway
(1) Elevation of the activation threshold
When antigenic stimulation is weak or costimulation is limited, CTLA4 more readily maintains T cells in a low-responsiveness state.
(2) Restriction of clonal expansion
Once T cells have been primed, CTLA4 can function as a negative feedback module to limit sustained expansion and prevent uncontrolled amplification of immune responses.
(3) Maintenance of peripheral tolerance
In the maintenance of self-tolerance and immune homeostasis, CTLA4 is central to peripheral tolerance by restricting aberrant activation and supporting Treg-mediated suppression.
5 Functional Differences of CTLA4 Across Distinct T-cell Subsets
5.1 Conventional CD4+ T Cells
(1) Post-activation feedback inhibition
In conventional CD4+ T cells, CTLA4 acts mainly as a negative feedback factor induced after activation to limit continued proliferation and cytokine production.
(2) Regulation of helper T-cell differentiation
CTLA4 not only reduces the magnitude of expansion but also affects the intensity and duration of differentiation programs in effector helper T-cell subsets such as Th1 and Th17 cells.
5.2 CD8+ T Cells
(1) Regulation of the initial priming threshold
In CD8+ T cells, CTLA4-mediated inhibition is more prominently reflected during the initial activation stage, especially under conditions strongly dependent on antigen presentation and costimulation.
(2) Context-dependent effects on effector maintenance
Across different infection, tumor, and immunointervention models, the extent to which CTLA4 affects CD8+ T-cell effector maintenance varies, but its role in restricting the priming threshold is comparatively consistent.
5.3 Treg Cells
(1) Core effector molecule of suppressive function
In Treg cells, CTLA4 is not an accessory molecule but one of the core suppressive mechanisms. Loss of CTLA4 markedly impairs the ability of Treg cells to suppress APCs and neighboring T cells.
(2) APC remodeling capacity
Through CTLA4, Treg cells downregulate CD80 and CD86 on APCs, creating a local microenvironment with insufficient costimulation and thereby limiting further expansion of effector T cells.
(3) Characteristics of outwardly directed immunosuppression
Unlike conventional T cells, in which CTLA4 primarily acts through self-feedback, CTLA4 in Treg cells more prominently exhibits trans-cellular regulatory properties, indirectly suppressing overall immune responses by remodeling APC state.
6 Biological Significance of the CTLA4 Pathway in Disease
6.1 Autoimmunity and Loss of Immune Tolerance
(1) Functional insufficiency and widespread immune activation
When CTLA4 expression, surface localization, or functional integrity is impaired, T cells are more likely to overcome the costimulatory threshold, leading to aberrant activation, lymphocyte expansion, and breakdown of peripheral tolerance.
(2) Multisystem involvement
Immune dysregulation associated with CTLA4 abnormalities is typically not confined to a single organ, but may involve the intestine, lung, hematopoietic system, lymphoid tissues, endocrine organs, and other sites.
6.2 Tumor Immunity
(1) Elevation of the tumor immune priming threshold
Within tumor-associated lymphoid tissues and draining lymph nodes, CTLA4 can limit the initial activation and expansion of tumor-specific T cells, thereby lowering the strength of antitumor immune priming.
(2) Enhancement of the Treg-mediated suppressive tumor environment
Treg cells enriched in tumor tissues often continuously weaken APC costimulatory capacity through CTLA4, thereby sustaining a locally suppressive immune state.
6.3 Infection and Inflammation
(1) Limitation of tissue damage
In late-stage infection or persistent inflammatory settings, CTLA4 can limit excessive T-cell activation and reduce immune-mediated tissue injury.
(2) Influence on pathogen clearance efficiency
If CTLA4 signaling is excessively strong, effector T-cell expansion may be insufficient, thereby reducing pathogen clearance efficiency. The role of CTLA4 in infection is therefore highly context-dependent.
7 Experimental Observation and Interpretation of CTLA4 Pathway Activity
7.1 Common Readouts
(1) CTLA4 expression status
This includes total protein, intracellular expression, and surface expression. For CTLA4, a high intracellular total level does not necessarily indicate strong surface function, so these three dimensions should be assessed separately.
(2) Availability of CD80 and CD86
If the focus is CTLA4-mediated regulation of APCs, analysis should not be restricted to the T-cell compartment; changes in the surface density of CD80 and CD86 on APCs should also be measured.
(3) T-cell activation readouts
IL-2, CD25, CD69, cell proliferation, pAKT, and mTOR activation status can all serve as functional readouts of CTLA4 pathway activity.
(4) Treg suppressive function readouts
When investigating the role of CTLA4 in immunosuppression, Treg suppression assays, APC coculture systems, and ligand depletion assays generally provide greater interpretive power than expression analysis alone.
7.2 Common Biases in Data Interpretation
(1) Equating expression with function
Increased CTLA4 expression does not necessarily mean enhanced inhibitory function. If CTLA4 is mainly retained intracellularly or its trafficking is impaired, functional surface expression may remain insufficient.
(2) Ignoring the CD28 background
The functional effect of the CTLA4 pathway is highly dependent on the strength of CD28-mediated costimulation. If baseline costimulation is already extremely weak, the gain achieved by CTLA4 blockade may not be substantial.
(3) Confounding contributions from different cell subsets
CTLA4 effects observed in whole samples often include major contributions from Treg cells. Without separating cell subsets, it is easy to misassign the source and level of signaling effects.
Table 3. Key Experimental Readouts for Analysis of the CTLA4 Pathway
Observation Level | Common Indicators | Methodological Significance |
Receptor expression | Surface CTLA4, intracellular CTLA4, total protein | Assess expression and trafficking status |
Ligand level | Changes in CD80 and CD86 density | Determine whether APC costimulatory resources are being depleted |
T-cell activation | IL-2, CD25, proliferation, pAKT | Assess the strength of costimulatory suppression |
Treg function | Suppression assays, APC coculture, ligand depletion | Assess trans-cellular regulatory capacity |
Therapeutic response | T-cell expansion, tumor infiltration, immune toxicity | Evaluate consequences of pathway intervention |
Table 4. Products Relevant to CTLA4 Pathway Research
Corresponding Research Module | Catalog No. | Name | Grade and Purity | Suitable Research Direction/Application |
MHC antigen presentation | MHC binding peptide | Moligand™ | Suitable for constructing MHC-loaded antigen systems for upstream antigen-presentation and T-cell activation studies in the CTLA4 pathway | |
MHC antigen presentation | Recombinant Human MHCA Protein | ≥90%(SDS-PAGE) | Suitable for MHC-related antigen presentation and ligand recognition studies | |
MHC I detection | MHC Class I/H-2 Rat mAb | Carrier Free,ExactAb™,Azide Free,Validated,PBS Only,≥95%(SDS-PAGE),See COA | Suitable for detection of MHC I expression and analysis of antigen-presentation status in APCs or target cells in CTLA4-related studies | |
MHC II detection | MHC Class II Rat mAb | Carrier Free,ExactAb™,Azide Free,Validated,PBS Only,See COA | Suitable for detecting MHC II expression and evaluating the activation state of antigen-presenting cells | |
MHC II detection | MHC Class II Rat mAb (APC) | ExactAb™, Validated, Ex:650nm, Em:660nm, 0.5 mg/mL | Suitable for flow-cytometric detection of MHC II expression | |
MHC II detection | MHC Class II Rat mAb (Biotin) | ExactAb™, Validated, 0.5 mg/mL | Suitable for biotin-labeled MHC II detection systems | |
MHC II detection | MHC Class II Rat mAb (FITC) | ExactAb™, Validated, Ex:498nm, Em:517nm, 0.5 mg/mL | Suitable for flow-cytometric detection of MHC II expression | |
MHC II detection | MHC Class II Rat mAb (PE) | ExactAb™, Validated, Ex:565nm, Em:575nm, 0.5 mg/mL | Suitable for flow-cytometric detection of MHC II expression | |
MHC I detection | MHC class I Mouse mAb | Carrier Free,Azide Free,Validated,PBS Only,≥95%(SDS-PAGE),See COA | Suitable for mouse MHC I expression detection | |
MHC I detection | MHC class I Mouse mAb (AF647) | ExactAb™, Validated, Ex:650nm, Em:668nm, 0.5 mg/mL | Suitable for flow-cytometric detection of MHC I expression | |
MHC I detection | MHC class I Mouse mAb (APC) | ExactAb™, Validated, Ex:650nm, Em:660nm, 0.5 mg/mL | Suitable for flow-cytometric detection of MHC I expression | |
MHC I detection | MHC class I Mouse mAb (Biotin) | ExactAb™, Validated, 0.5 mg/mL | Suitable for biotin-labeled MHC I detection systems | |
MHC I detection | MHC class I Mouse mAb (FITC) | ExactAb™, Validated, Ex:498nm, Em:517nm, 0.5 mg/mL | Suitable for flow-cytometric detection of MHC I expression | |
MHC I detection | MHC class I/H-2Kb Mouse mAb | Carrier Free,ExactAb™,Azide Free,Validated,PBS Only,≥95%(SDS-PAGE),See COA | Suitable for antigen-presentation analysis in the H-2Kb mouse background | |
MHC I detection | MHC class I/H-2Kb Mouse mAb | Carrier Free,ExactAb™,Azide Free,Validated,PBS Only,≥95%(SDS-PAGE),See COA | Suitable for antigen-presentation analysis in the H-2Kb mouse background | |
MHC I detection | MHC class I/H-2Kb Mouse mAb (AF488) | ExactAb™, Validated, 0.5 mg/mL | Suitable for flow-cytometric H-2Kb detection | |
MHC I detection | MHC class I/H-2Kb Mouse mAb (AF647) | ExactAb™, Validated, Ex:650nm, Em:668nm, 0.5 mg/mL | Suitable for flow-cytometric H-2Kb detection | |
MHC I detection | MHC class I/H-2Kb Mouse mAb (AF700) | ExactAb™, Validated, 0.5 mg/mL | Suitable for H-2Kb detection in multicolor flow cytometry | |
MHC I detection | MHC class I/H-2Kb Mouse mAb (Biotin) | ExactAb™, Validated, 0.5 mg/mL | Suitable for biotin-labeled H-2Kb detection | |
MHC I detection | MHC class I/H-2Kb Mouse mAb (FITC) | ExactAb™, Validated, Ex:498nm, Em:517nm, 0.5 mg/mL | Suitable for flow-cytometric H-2Kb detection | |
MHC I detection | MHC class I/H-2Kk Mouse mAb | Carrier Free,ExactAb™,Azide Free,Validated,PBS Only,≥95%(SDS-PAGE),See COA | Suitable for antigen-presentation studies associated with the H-2Kk subtype | |
MHC II detection | MHC class II I E kappa Mouse mAb | Carrier Free,Azide Free,Validated,PBS Only,≥95%(SDS-PAGE),See COA | Suitable for mouse MHC II expression detection | |
MHC II detection | MHC class II I E kappa Mouse mAb (AF647) | ExactAb™, Validated, Ex:650nm, Em:668nm, 0.5 mg/mL | Suitable for flow-cytometric MHC II detection | |
MHC II detection | MHC class II I E kappa Mouse mAb (Biotin) | ExactAb™, Validated, 0.5 mg/mL | Suitable for biotin-labeled MHC II detection | |
MHC II detection | MHC class II I E kappa Mouse mAb (FITC) | ExactAb™, Validated, Ex:498nm, Em:517nm, 0.5 mg/mL | Suitable for flow-cytometric MHC II detection | |
MHC II detection | MHC class II I E kappa Mouse mAb (PE) | ExactAb™, Validated, Ex:565nm, Em:575nm, 0.5 mg/mL | Suitable for flow-cytometric MHC II detection | |
MHC II detection | Recombinant MHC Class II Antibody | Animal Free,Carrier Free,Recombinant,ExactAb™,Azide Free,Validated,High Performance,PBS Only,≥95%(SDS-PAGE),See COA | Suitable for MHC II detection and studies using recombinant antibody systems | |
MHC II detection | Recombinant MHC Class II Antibody (AF405) | 0.5 mg/mL | Suitable for MHC II detection in multicolor flow cytometry | |
MHC II detection | Recombinant MHC Class II Antibody (AF555) | ExactAb™, Validated, 0.5 mg/mL | Suitable for MHC II detection in multicolor flow cytometry | |
MHC II detection | Recombinant MHC Class II Antibody (AF647) | ExactAb™, Validated, 0.5 mg/mL | Suitable for MHC II detection in multicolor flow cytometry | |
MHC II detection | Recombinant MHC Class II Antibody (APC) | Validated, ExactAb™, 0.5 mg/mL | Suitable for MHC II detection in multicolor flow cytometry | |
MHC II detection | Recombinant MHC Class II Antibody (Biotin) | Validated, ExactAb™, 0.5 mg/mL | Suitable for biotin-labeled MHC II detection | |
MHC II detection | Recombinant MHC Class II Antibody (FITC) | ExactAb™, Validated, 0.5 mg/mL | Suitable for MHC II detection in multicolor flow cytometry | |
MHC II detection | Recombinant MHC Class II Antibody (PE) | ExactAb™, Validated, 0.5 mg/mL | Suitable for MHC II detection in multicolor flow cytometry | |
MHC II detection | Recombinant MHC Class II Antibody (PE-Cy5) | ExactAb™, Validated, 0.5 mg/mL | Suitable for MHC II detection in multicolor flow cytometry | |
MHC II detection | Recombinant MHC Class II Antibody (PerCP-Cy5.5) | ExactAb™, Validated, 0.5 mg/mL | Suitable for MHC II detection in multicolor flow cytometry | |
Total TCR detection | TCR beta Armenian Hamster mAb | Carrier Free,ExactAb™,Azide Free,Validated,PBS Only,See COA | Suitable for TCRβ-chain detection and analysis of TCR-dependent activation background | |
Total TCR detection | TCR α/β Mouse mAb | Carrier Free,Azide Free,Validated,PBS Only,≥95%(SDS-PAGE),See COA | Suitable for overall αβ T-cell identification and phenotypic analysis | |
Total TCR detection | TCR α/β Mouse mAb (AF647) | ExactAb™, Validated, Ex:650nm, Em:668nm, 0.5 mg/mL | Suitable for flow-cytometric detection of αβ T cells | |
Total TCR detection | TCR α/β Mouse mAb (APC) | ExactAb™, Validated, Ex:650nm, Em:660nm, 0.5 mg/mL | Suitable for flow-cytometric detection of αβ T cells | |
Total TCR detection | TCR α/β Mouse mAb (Biotin) | ExactAb™, Validated, 0.5 mg/mL | Suitable for biotin-labeled detection of αβ T cells | |
Total TCR detection | TCR α/β Mouse mAb (FITC) | ExactAb™, Validated, Ex:498nm, Em:517nm, 0.5 mg/mL | Suitable for flow-cytometric detection of αβ T cells | |
Total TCR detection | TCR α/β Mouse mAb (PE) | ExactAb™, Validated, 0.5 mg/mL | Suitable for flow-cytometric detection of αβ T cells | |
Total TCR detection | TCR γ/δ Armenian Hamster mAb | Carrier Free, Azide Free, Validated, ≥95%(SDS-PAGE), See COA | Suitable for overall γδ T-cell identification | |
Total TCR detection | TCR γ/δ Mouse mAb | Carrier Free,Azide Free,Validated,PBS Only,≥95%(SDS-PAGE),See COA | Suitable for overall γδ T-cell identification | |
Total TCR detection | TCR γ/δ Mouse mAb (AF488) | ExactAb™, Validated, 0.5 mg/mL | Suitable for flow-cytometric detection of γδ T cells | |
Total TCR detection | TCR γ/δ Mouse mAb (AF647) | ExactAb™, Validated, 0.5 mg/mL | Suitable for flow-cytometric detection of γδ T cells | |
Total TCR detection | TCR γ/δ Mouse mAb (APC) | ExactAb™, Validated, 0.5 mg/mL | Suitable for flow-cytometric detection of γδ T cells | |
Total TCR detection | TCR γ/δ Mouse mAb (Biotin) | ExactAb™, Validated | Suitable for biotin-labeled detection of γδ T cells | |
Total TCR detection | TCR γ/δ Mouse mAb (PE) | ExactAb™, Validated, 0.5 mg/mL | Suitable for flow-cytometric detection of γδ T cells | |
Total TCR detection | Recombinant TCR γ/δ Antibody | Animal Free,Carrier Free,Recombinant,ExactAb™,Azide Free,Validated,High Performance,PBS Only,≥95%(SDS-PAGE),See COA | Suitable for γδ T-cell detection and studies using recombinant antibody systems | |
Total TCR detection | Recombinant TCR γ/δ Antibody | Animal Free,Carrier Free,Recombinant,ExactAb™,Azide Free,Validated,High Performance,PBS Only,≥95%(SDS-PAGE),See COA | Suitable for γδ T-cell detection and studies using recombinant antibody systems | |
Total TCR detection | Recombinant TCR γ/δ Antibody (AF405) | ExactAb™, Validated, Recombinant, 0.5mg/mL | Suitable for multicolor flow-cytometric detection of γδ T cells | |
Total TCR detection | Recombinant TCR γ/δ Antibody (AF488) | ExactAb™, Validated, Recombinant, 0.5mg/mL | Suitable for multicolor flow-cytometric detection of γδ T cells | |
Total TCR detection | Recombinant TCR γ/δ Antibody (AF488) | ExactAb™, Validated, 5 μL/test | Suitable for flow-cytometric detection of γδ T cells | |
Total TCR detection | Recombinant TCR γ/δ Antibody (AF647) | ExactAb™, Validated, 5 μL/test | Suitable for flow-cytometric detection of γδ T cells | |
Total TCR detection | Recombinant TCR γ/δ Antibody (APC) | ExactAb™, Validated, Recombinant, 0.5mg/mL | Suitable for multicolor flow-cytometric detection of γδ T cells | |
Total TCR detection | Recombinant TCR γ/δ Antibody (FITC) | ExactAb™, Validated, 5 μL/test | Suitable for flow-cytometric detection of γδ T cells | |
TCR subset phenotyping | TCR V Gamma 2 Armenian Hamster mAb | Carrier Free,ExactAb™,Azide Free,Validated,PBS Only,≥95%(SDS-PAGE),See COA | Suitable for analysis of specific TCR γ-chain subsets | |
TCR subset phenotyping | TCR V beta 4 Rat mAb | Carrier Free,ExactAb™,Azide Free,Validated,PBS Only,≥95%(SDS-PAGE),See COA | Suitable for TCR Vβ4 subset analysis | |
TCR subset phenotyping | TCR V beta 8 Mouse mAb | Carrier Free,ExactAb™,Azide Free,Validated,PBS Only,≥95%(SDS-PAGE),See COA | Suitable for TCR Vβ8 subset analysis | |
TCR subset phenotyping | TCR Valpha24-Jalpha18 (iNKT cell) Mouse mAb | Carrier Free,ExactAb™,Low Endotoxin,Azide Free,Validated,PBS Only,≥95%(SDS-PAGE&HPLC),1.0-5.0 mg/mL | Suitable for iNKT-cell identification and subset analysis | |
TCR subset phenotyping | TCR Valpha24-Jalpha18 (iNKT cell) Mouse mAb (AF488) | ExactAb™, Validated, 5 μL/test | Suitable for flow-cytometric detection of iNKT cells | |
TCR subset phenotyping | TCR Valpha24-Jalpha18 (iNKT cell) Mouse mAb (AF647) | ExactAb™, Validated, Ex:650nm, Em:668nm, 5 μL/test | Suitable for flow-cytometric detection of iNKT cells | |
TCR subset phenotyping | TCR Valpha24-Jalpha18 (iNKT cell) Mouse mAb (Biotin) | ExactAb™, Validated, 0.5 mg/mL | Suitable for biotin-labeled detection of iNKT cells | |
TCR subset phenotyping | TCR Valpha24-Jalpha18 (iNKT cell) Mouse mAb (FITC) | ExactAb™, Validated, Ex:498nm, Em:517nm, 5 μL/test | Suitable for flow-cytometric detection of iNKT cells | |
TCR subset phenotyping | TCR Valpha24-Jalpha18 (iNKT cell) Mouse mAb (PE) | ExactAb™, Validated, 5 μL/test | Suitable for flow-cytometric detection of iNKT cells | |
TCR subset phenotyping | TCR Vγ1.1/Cr4 Armenian hamster mAb | Carrier Free,ExactAb™,Azide Free,Validated,PBS Only,≥95%(SDS-PAGE),See COA | Suitable for analysis of specific γδ T-cell subsets | |
TCR subset phenotyping | TCR Vγ1.1/Cr4 Armenian hamster mAb (APC) | ExactAb™, Validated, Ex:650nm, Em:660nm, 0.5 mg/mL | Suitable for flow-cytometric detection of γδ T-cell subsets | |
TCR subset phenotyping | TCR Vγ1.1/Cr4 Armenian hamster mAb (Biotin) | ExactAb™, Validated, 0.5 mg/mL | Suitable for biotin-labeled detection of γδ T-cell subsets | |
TCR subset phenotyping | TCR Vγ1.1/Cr4 Armenian hamster mAb (FITC) | ExactAb™, Validated, Ex:498nm, Em:517nm, 0.5 mg/mL | Suitable for flow-cytometric detection of γδ T-cell subsets | |
TCR subset phenotyping | TCR Vγ1.1/Cr4 Armenian hamster mAb (PE) | ExactAb™, Validated, Ex:565nm, Em:575nm, 0.5 mg/mL | Suitable for flow-cytometric detection of γδ T-cell subsets | |
Upstream stimulation tool | TOL101 (anti-TCR) | Carrier Free, Recombinant, ExactAb™, Low Endotoxin, Azide Free, Validated, Animal Free, ≥95%(SDS-PAGE&SEC-HPLC), See COA | Suitable for construction of TCR intervention and upstream stimulation/blockade models | |
Proximal signaling readout | Recombinant LAT Antibody | ExactAb™, Validated, Recombinant, 0.2 mg/mL | Suitable for LAT detection as a proximal TCR signaling activation readout |
The core function of the CTLA4 pathway lies in fine control over T-cell costimulatory resources and the threshold of immune activation. Its role is reflected not only in suppression of intracellular activation programs in T cells, but also in reshaping the immune microenvironment through regulation of ligand availability on antigen-presenting cells.
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