In vivo studies have been hindered by the lack of orthologous proteins in mice. Humanized or transgenic mice are used to overcome this discrepancy and some studies use different animal species. Their function in Mycobacterium tuberculosis infection has been the main focus in past research.<unk>  are more similar to conventional T<unk>  because their response takes days to weeks and they exhibit an accelerated response after prior immunization. This differs from their<unk>  2 counterparts (Natural killer T ceCortical thymocyteslls) which react swiftly but undergo anergy following reexposure. Mycobacterium tuberculosis infection Many lipid antigens of Mycobacterium tuberculosis have been indentified, including: mycolic acid, glucose and glycerol monomycolates, lipoarabinomannan, phosphatidylinositol mannoside, diacylsulfoglycolipid, mannosyl-β-1-phosphomycoketide and didehydroxymycobactin. Most of these antigens are bound to<unk> b.<unk>  are activated after Mycobacterium infection and produce IFN-γ and TNF-α (Th1 type response). These<unk>  can be double negative (CD4-CD8-), CD4+ or CD8+ and possess strong cytotoxic capabilities. Studies using<unk> b tetramers presenting the mycobacterial product glucose monomycolate identified two CD4+ TCRαβ+ T<unk> populations which differ from the otherwise variable TCR composition of previously isolated subsets, one termed 'GEM (Germline-encoded, mycolyl-reactive)' for their conserved TCR repertoire (specifically TRAV1-2+TRAJ9+) and 'LDN5-like' (TRBV4-1+). These<unk>  are rare in individuals that have not encountered Mycobacterium tuberculosis.<unk>  expression is downregulated in antigen presenting<unk>  infected with live Mycobacteria, perhaps as a means of immune evasion. This downregulation can be also found in some leukemia<unk> . Autoreactivity<unk>  can be activated by endogenous lipids, including gangliosides (GM1,GD1a, GD1b, GT1b, and GQ1b), sulfatides, sphingomyelin, phophatidylglycerol, lysophospholipids, squalene, wax esters, and triacylglycerides. Methyl-lysophosphatidic acids (mLPAs) are rare in healthy monocytes and B<unk>  but are abundant in leukemic<unk> .<unk> c self-reactive T<unk>  were found to kill acute leukemia<unk>  expressing<unk> c binding these lipids.<unk> a self-reactive T<unk>  were found in the blood of healthy individuals. These<unk>  express skin-homing receptors and produce interleukin 22 after binding<unk> a on Langerhans<unk> .<unk> a binds many endogenous lipids found in skin-oil and is able to activate T-cells even with ligands that lack a hydrophilic part, e.g. squalene. CD8+ TCR αβ+<unk> b T<unk>  have been found in the central nervous system of patients with multiple sclerosis. They recognized glycolipids and secreted IFN-γ and TNF-α. Other autoimmune diseases where<unk>  might contribute include psoriasis and systemic lupus erythematosus.
Group 1 CD1-restricted T cells
Persistent polyclonal B-cell lymphocytosis
Mutated citrullinated vimentin
Chimeric antigen receptor T cell
IgG4-related skin disease
Cross-reactive carbohydrate determinants
Deficiency of the interleukin-1–receptor antagonist
Antibodies from lymphocyte secretions