Disease relevance of Atp8a2

• Subclinical infection of BALB/c mice with the intracellular pathogen Listeria monocytogenes results in the development of MHC class Ia- and Ib-restricted CTLs [1].
• The expression of the foreign gene ibp, encoding the Ib component of iota toxin from Clostridium perfringens, was analyzed [2].
• Ribonucleotide reduction in Mycobacterium tuberculosis: function and expression of genes encoding class Ib and class II ribonucleotide reductases [3].
• A recombinant Bacillus anthracis strain producing the Clostridium perfringens Ib component induces protection against iota toxins [2].
• In the past 4 years, genes mutated in Usher syndrome type Ib and type IIa have been described [4].

High impact information on Atp8a2

• Murine T10 and T22 are highly related nonclassical major histocompatibility complex (MHC) class Ib proteins that bind to certain gammadelta T cell receptors (TCRs) in the absence of other components [5].
• Transporters associated with antigen processing (TAP)-independent presentation of soluble insulin to alpha/beta T cells by the class Ib gene product, Qa-1(b) [6].
• Therefore, this class Ib protein may have access to a novel antigen processing pathway that is not available to class Ia molecules [6].
• Advances have been made in understanding the expression of the non-classical HLA class Ib genes and work with the murine class Ib proteins has demonstrated that these antigens can present a specialized subset of peptides to the immune system [7].
• These results demonstrate that TCR gamma/delta cells have the capacity to cause acute lethal GVHD in mice and suggest that nonclassical MHC class Ib gene products expressed on GVHD target organs are responsible for G8 Tg TCR gamma/delta+ cell mediated lethality [8].

Biological context of Atp8a2

• The mutation does not affect transcription of the Ib-IX genes, as estimated by PCR and Northern blot analysis, but it does inhibit surface expression of the receptor as assessed by transient transfection of mutant and wild-type GPIb alpha genes into mouse Ib beta-IX L cells [9].
• A non-overlapping set of three class Ib cDNA clones was obtained from the fetal liver, including T13c, the Thy 19.4 gene, and a previously uncharacterized class I gene provisionally designated as FL 57 [10].
• 2. Although the majority of H-2Dd cDNA clones that were analyzed lack introns, many of the class Ib cDNA clones contain intron sequences [10].
• Of the 29 total class Ib genes, transcripts of five including Q6d, Q7d, T9c, T10c, and the 37 gene were isolated from the bone marrow cDNA library [10].
• Mice given injections of live BAIB spores developed an antibody response specific to the Ib protein [2].

Anatomical context of Atp8a2

• The major histocompatibility complex class Ib protein, Qa-1(b), serves as a ligand for murine CD94/NKG2A natural killer (NK) cell inhibitory receptors [11].
• L. monocytogenes-infected B6.Tla(a)-derived bone marrow macrophages (Kb Qa-1a) are not lysed by BALB/c (Kd Qa-1b)-derived antilisterial CTLs, confirming an earlier finding that the Ib-restricting element is T region encoded [1].
• The gastrointestinal tract is populated by a multitude of specialized immune cells endowed with receptors for classical (class Ia) and nonclassical (class Ib) MHC proteins [12].
• L. monocytogenes-infected TAP-/- bone marrow macrophage targets are not lysed by MHC class Ia- or Ib-restricted CTLs, showing a requirement for transport of peptides into the endoplasmic reticulum for development of the MHC class Ib-peptide target [1].
• Expression of Qa-2 in the corneal endothelium and other substructures lining the anterior chamber suggests that this class Ib protein may contribute to the immune-privileged status of the anterior chamber [13].

Associations of Atp8a2 with chemical compounds

• The H2-M3 class Ib gene product, M3, preferentially presents formylmethionine-initiating (fMet) peptides derived from the N termini of bacterial and mitochondrial proteins [14].
• Murine MHC class Ib gene, H2-M2, encodes a conserved surface-expressed glycoprotein [15].

Analytical, diagnostic and therapeutic context of Atp8a2

• Five monoclonal antibodies against Ib were also tested with each truncated Ib variant for epitope and structural mapping by surface plasmon resonance and an enzyme-linked immunosorbent assay [16].
• The increased cell surface expression of these antigens as well as induction of the genes mentioned above as measured by RT-PCR suggests that JEV infection may lead to the induction of classical MHC Class Ia as well as nonclassical MHC Class Ib molecules [17].

References