KLRK1 Specific Neutra™ Antibody Products

KLRK1 (Killer Cell Lectin Like Receptor K1) is a member of the NKG2 family, distinguished by a type II membrane topology featuring an extracellular C-terminal region and incorporating a C-type lectin domain. It engages with a broad spectrum of ligands, encompassing MICA/B proteins as well as ULBP. These interactions can activate T and NK cells. Surface expression of these ligands plays a crucial role in immune system's recognition of stressed cells, making KLRK1 and its ligands potential targets for therapeutic interventions in the immune disorders and cancer.

Its Gene ID: 22914, UniProtKB ID: P26718, and OMIM ID: 611817.

KLRK1 Related Pathway

The role of KLKR2 in NK cell cytotoxicity involves binding to stress-inducible counterparts of HLA class I, specifically MICA/B molecules. KLKR2, also known as NKG2D, activates multiple intracellular pathways in NK cells through interaction with its ligand, facilitated by the DAP10 signaling molecule. Activation of NK cell cytotoxicity can occur via pathways involving PLCγ2, JNK, and phosphatidylinositol 3-kinase (PI3K). PLCγ2 and PI3K pathways trigger granule release, while the JAK-STAT5 pathway induces cytokine secretion.

Fig.1 Activation of KLRK1/NKG2D-related pathways.^{1, 2}

Applications of Anti-KLRK1 Antibodies

• Role of Anti-KLRK1 Antibodies in AML Treatment

KLRK1 plays a pivotal role in the activation of NK cells for the elimination of hematological malignant cell lines. Various hematological malignant cell lines are used as targets, and the expression levels of MICA and MICB, ligands for KLRK1, are assessed by flow cytometry. NK cell line is co-incubated with either an isotype control antibody or an anti-KLRK1 blocking antibody, which specifically inhibits KLRK1, and then co-cultured with the different target cell lines. Following incubation, the apoptotic ratio of each target cell line is assessed via flow cytometry. The results show a significant reduction in the apoptotic ratio of acute myeloid leukemia (AML) cell line when target NK cells are pre-incubated with the KLRK1 blocking antibody. These findings indicate that KLRK1 can activate NK cells by inducing cytotoxicity in specific target cells by inducing cytotoxicity in specific target cells.

• Anti-KLRK1 MAb Demonstrates KLRK1-Mediated CD8⁺ T Cells Costimulation

CD8⁺ T cell activation needs both a costimulatory signal and TCR engagement. KLRK1 has been implicated in T cell costimulation. However, naive or effector CD8⁺ T cell responses in conventional T cell populations are insufficient to be costimulated by the engagement of KLRK1 by its ligand or by anti-KLRK1 monoclonal antibody (mAb). Although KLRK1 alone does not costimulate CD8⁺ T cells, it can modulate CD28-mediated costimulation of human CD8⁺ T cells under specific conditions. Thus, KLRK1 is likely to function as a costimulatory molecule only in the presence of additional cofactors or under specific conditions. This finding has generated significant interest in tumor biology, autoimmunity, and infectious diseases. KLRK1 may be a potential candidate for therapeutic targeting to inhibit autoimmune T cells or enhance T cell responses to tumors or pathogen-infected tissues.

Creative Biolabs provides a range of meticulously engineered antibodies targeting KLRK1, developed using state-of-the-art recombinant technologies. Furthermore, bespoke customization services are available to design neutralizing antibodies targeting KLRK1, tailored to precise specifications.

REFERENCES

1. Siemaszko, Jagoda, Aleksandra Marzec-Przyszlak, and Katarzyna Bogunia-Kubik. "NKG2D natural killer cell receptor—a short description and potential clinical applications." Cells 10.6 (2021): 1420.
2. Distributed Under open access license CC BY 4.0, without modification.