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| - | *[[Beta-2 microglobulin|Beta-2 microglobulin]] | ||
== References == | == References == | ||
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Revision as of 08:25, 15 November 2017
Crystal Structure of C12C TCR-HA B2705-KK10
Structural highlights
Disease[1B27_HUMAN] Defects in HLA-B are a cause of susceptibility to spondyloarthropathy type 1 (SPDA1) [MIM:106300]. It is a chronic rheumatic disease with multifactorial inheritance. It includes a spectrum of related disorders comprising ankylosing spondylitis, a subset of psoriatic arthritis, reactive arthritis (e.g. Reiter syndrome), arthritis associated with inflammatory bowel disease and undifferentiated spondyloarthropathy. These disorders may occur simultaneously or sequentially in the same patient, probably representing various phenotypic expressions of the same disease. Ankylosing spondylitis is the form of rheumatoid arthritis affecting the spine and is considered the prototype of seronegative spondyloarthropathies. It produces pain and stiffness as a result of inflammation of the sacroiliac, intervertebral, and costovertebral joints. Note=In the Greek Cypriot population, a restricted number of HLA-B27 subtypes are associated with ankylosing spondylitis and other B27-related diseases and an elevated frequency of the B*2702 allele in ankylosing spondylitis patients is identified. The allele B*2707 seems to have a protective role in this population because it was found only in the healthy controls.[1] [B2MG_HUMAN] Defects in B2M are the cause of hypercatabolic hypoproteinemia (HYCATHYP) [MIM:241600]. Affected individuals show marked reduction in serum concentrations of immunoglobulin and albumin, probably due to rapid degradation.[2] Note=Beta-2-microglobulin may adopt the fibrillar configuration of amyloid in certain pathologic states. The capacity to assemble into amyloid fibrils is concentration dependent. Persistently high beta(2)-microglobulin serum levels lead to amyloidosis in patients on long-term hemodialysis.[3] [4] [5] [6] [7] [8] [9] [10] [11] [12] [13] [14] [15] Function[1B27_HUMAN] Involved in the presentation of foreign antigens to the immune system. [B2MG_HUMAN] Component of the class I major histocompatibility complex (MHC). Involved in the presentation of peptide antigens to the immune system. Publication Abstract from PubMedThe capacity of the immune system to adapt to rapidly evolving viruses is a primary feature of effective immunity, yet its molecular basis is unclear. Here, we investigated protective HIV-1-specific CD8(+) T cell responses directed against the immunodominant p24 Gag-derived epitope KK10 (KRWIILGLNK263-272) presented by human leukocyte antigen (HLA)-B( *)2705. We found that cross-reactive CD8(+) T cell clonotypes were mobilized to counter the rapid emergence of HIV-1 variants that can directly affect T cell receptor (TCR) recognition. These newly recruited clonotypes expressed TCRs that engaged wild-type and mutant KK10 antigens with similar affinities and almost identical docking modes, thereby accounting for their antiviral efficacy in HLA-B( *)2705(+) individuals. A protective CD8(+) T cell repertoire therefore encompasses the capacity to control TCR-accessible mutations, ultimately driving the development of more complex viral escape variants that disrupt antigen presentation. A Molecular Basis for the Control of Preimmune Escape Variants by HIV-Specific CD8(+) T Cells.,Ladell K, Hashimoto M, Iglesias MC, Wilmann PG, McLaren JE, Gras S, Chikata T, Kuse N, Fastenackels S, Gostick E, Bridgeman JS, Venturi V, Arkoub ZA, Agut H, van Bockel DJ, Almeida JR, Douek DC, Meyer L, Venet A, Takiguchi M, Rossjohn J, Price DA, Appay V Immunity. 2013 Mar 21;38(3):425-36. doi: 10.1016/j.immuni.2012.11.021. PMID:23521884[16] From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine. References
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Categories: Human | Gras, S | Rossjohn, J | Wilmann, P G | Hiv | Hla b*2705 | Immune escape | Immune system | Kk10 | T cell | Tcr
