Phosphatidylserine receptor that plays different role in immune response including phagocytosis of apoptotic cells and T-cell regulation (PubMed:17960135). Controls T-cell activation in a bimodal fashion, decreasing the activation of naive T-cells by inducing cell cycle arrest, while increasing proliferation of activated T-cells by activating AKT1 and ERK1/2 phosphorylations and subsequent signaling pathways. Also plays a role in efferocytosis which is the process by which apoptotic cells are removed by phagocytic cells (PubMed:18354194, PubMed:18367551). Mechanistically, promotes the engulfment of apoptotic cells or exogenous particles by securing them to phagocytes through direct binding to phosphatidylserine present on apoptotic cells, while other engulfment receptors such as MERTK efficiently recognize apoptotic cells and mediate their ingestion (By similarity). Additionally, promotes autophagy process by suppressing NLRP3 inflammasome activity via activation of STK11/PRKAA1 pathway in a phosphatidylserine-dependent mechanism (PubMed:31263038). Homodimer. Predominantly expressed in lymphoid tissues, such as spleen, lymph nodes, and Peyer patches. Also expressed in fetal liver, salivary gland, and spleen stromal cells, predominantly in the marginal zone and to a lesser extent throughout the white pulp. Not expressed in bone marrow-derived cells. Expressed mainly by antigen presenting cells (APCs) in T- and B-cell areas, but not by T- or B-lymphocytes. Down-regulated in lymphotoxin deficient mice. Deletion mice maintained on methionine and choline-deficient diet exhibit significantly more obvious inflammation and severe lipid accumulation. Belongs to the T-cell and airway phenotype regulator (Tapr) locus, a single chromosomal region that confers reduced T-helper type 2 responsiveness and protects against airway hyperactivity (AHR), the hallmark of human asthma. Low expression of Timd4 is associated with lymphotoxin deficiency. Belongs to the immunoglobulin superfamily. TIM family.