The KLRC1 gene encodes NKG2A, a transmembrane protein belonging to the C-type lectin-like family, primarily expressed on natural killer (NK) cells and a subset of cytotoxic T cells. As an inhibitory receptor, NKG2A forms heterodimers with CD94 to recognize the non-classical MHC class I molecule HLA-E. This interaction delivers suppressive signals that regulate immune cell activity, preventing excessive cytotoxicity and maintaining immune homeostasis. KLRC1 antibodies are critical tools for studying NK/T cell function, immune evasion mechanisms in cancer, and viral infections (e.g., HIV, CMV) where pathogens upregulate HLA-E to evade detection.
In research, anti-KLRC1 antibodies enable flow cytometry-based immunophenotyping, immunohistochemical staining of tissue samples, and functional studies blocking NKG2A-CD94/HLA-E interactions. They’re pivotal in exploring therapeutic strategies, particularly in oncology, where NKG2A blockade is investigated to enhance antitumor immunity. Clinical-stage inhibitors like monalizumab (anti-NKG2A) exemplify translational applications, showing promise in combination therapies with checkpoint inhibitors. Structurally, these antibodies often target extracellular domains of NKG2A, requiring careful validation for specificity due to homology with other NKG2 family members (e.g., NKG2C). Current studies also focus on KLRC1 polymorphisms linked to disease susceptibility, emphasizing its dual role in protective immunity and pathological tolerance.