Key facts
Reacts with:Human,
Target:PDCD1See target data
Product details:
Immune Checkpoint Inhibitors Panel - Human IHC ab278174 contains multiple trial-sized versions of anti-human antibody clones against PD-L1, PD1, LAG3, TIM 3, VISTA, CTLA4 and TIGIT specifically selected for high performance in various applications. They are provided as a sampler panel to allow you to easily evaluate each antibody.
For guidelines on how to use each antibody within the panel, please consult the individual datasheet for each antibody.
Panel contains:
- Rabbit monoclonal [73-10] to PD-L1 (20 μL)
ab228415
- Rabbit monoclonal [EPR4877(2)] to PD1 (20 μL)
ab137132
- Rabbit monoclonal [EPR20261] to LAG-3 (20 μL)
ab209236
- Rabbit monoclonal [EPR22241] to TIM 3 (20 μL)
ab241332
- Rabbit monoclonal [EPR21050] to VISTA (20 μL)
ab230950
- Rabbit monoclonal [CAL49] to CTLA4 (20 μL)
ab237712
- Rabbit monoclonal [BLR047F] to TIGIT - BSA free (20 μL)
ab243903
Explore our range of antibody sample panels designed to provide you with a variety of trial-size antibodies in a convenient and cost-effective format.
Carrier-free formulations of our recombinant antibodies are also available for easy conjugation to labels of your choice and for multiplex applications. Use our intuitive search and select carrier-free or your label of choice. For bespoke conjugations or large volumes email
[email protected].
Properties and Storage Information:
Shipped at conditions-Blue Ice, Appropriate short-term storage conditions--20°C, Appropriate long-term storage conditions--20°C, Storage information--20°C
Supplementary Information:
This supplementary information is collated from multiple sources and compiled automatically.
CTLA4 (Cytotoxic T-Lymphocyte–Associated protein 4) TIM 3 (T-cell immunoglobulin and mucin-domain containing-3) PD1 (Programmed cell death protein 1) LAG-3 (Lymphocyte Activation Gene-3) PD-L1 (Programmed death-ligand 1) VISTA (V-domain Ig suppressor of T cell activation) and TIGIT (T cell immunoreceptor with Ig and ITIM domains) are immune checkpoint molecules that play significant roles in immune regulation. They act as inhibitory receptors and ligands expressed on the surfaces of T cells and other immune cells modulating immune responses. For example CTLA4 has a mass of approximately 33 kDa and is primarily expressed on activated T cells while PD-L1 is found on B cells dendritic cells and some tumor cells. These molecules form an 'immune checkpoint panel' influencing T-cell receptor signaling cascades.
Biological function summary
These immune checkpoint molecules regulate immune activation and tolerance to prevent overactive immune responses. They interact with specific ligands to transmit inhibitory signals that reduce the proliferation of T cells and diminish cytokine production. CTLA4 competes with CD28 to bind B7 molecules thereby inhibiting T cell activation. PD1 interaction with PD-L1 results in the suppression of T cell activity in tissues. These interactions are essential components of the immune system's self-tolerance mechanisms often working as part of larger protein complexes.
Pathways
Immune checkpoints play integral roles in the immune regulation pathways that prevent autoimmune reactions and maintain immune homeostasis. CTLA4 and PD1 are linked to the T cell receptor (TCR) signaling pathway inhibiting activation signals through interactions with their ligands. They relate closely to proteins like CD28 which has opposing effects on T cell activation. Their regulation involves complex signaling cascades including SHP2 and PI3K pathways which further control immune cell responses.
Dysregulation of immune checkpoints contributes to tumor immune evasion in cancer and the development of autoimmune diseases. In cancer overexpression of PD-L1 on tumor cells interacts with PD1 dampening immune surveillance and promoting tumor growth. In autoimmune diseases reduced function of these checkpoints can lead to excessive immune activation and tissue damage. For instance in psoriasis altered expression patterns of CTLA4 and PD1 may exacerbate inflammatory pathways. Understanding these interactions offers therapeutic opportunities using checkpoint inhibitors to restore immune balance and improve patient outcomes.
