Disease relevance of BOLA

• The presence of class I major histocompatibility complex-restricted CTLs with potentially autoreactive specificities in preimmune animals raises the possibility of a role for such cells in autoimmune disease states [1].
• A major histocompatibility complex class I (BoLA-A) allele that has been previously associated with resistance to PL was associated with longevity and realization of milk production potentials, indicating that genetic resistance to PL will have an economic benefit in herds where BLV is endemic [2].
• We generated a recombinant influenza virus expressing an epitope from the circumsporozoite protein of P. yoelii known to be recognized by CD8+ T cells and demonstrated that this vector induced class I major histocompatibility complex-restricted cytotoxic T cells against this foreign epitope [3].
• Using a permeabilized cell system in which major histocompatibility complex class I heavy chains are retrotranslocated under the influence of the human cytomegalovirus protein US11, we demonstrate that polyubiquitination alone is insufficient to provide the driving force for retrotranslocation [4].
• Since malignant transformation of cells is associated with changes in structures coded by the MHC region, 10 cultured human melanoma and sarcoma cells and autologous SV40-transformed fibroblasts were tested for expression of MRBC receptors and compared with normal autologous fibroblasts [5].

High impact information on BOLA

• Major histocompatibility complex (MHC) glycoproteins bind processed fragments of proteins and present them to the receptors of T lymphocytes [6].
• Beta 2-microglobulin from serum associates with MHC class I antigens on the surface of cultured cells [7].
• Receptor-mediated uptake of antigen/heat shock protein complexes results in major histocompatibility complex class I antigen presentation via two distinct processing pathways [8].
• Although this antigenicity is known to arise from HSP-associated peptides presented to the immune system by major histocompatibility complex (MHC) class I molecules, the cell biology underlying this presentation process remains poorly understood [8].
• T cell hybridomas isolated from nonresponder H-2(b) mice immunized with pork insulin were stimulated by insulin in the presence of major histocompatibility complex (MHC)-unmatched antigen presenting cells [9].

Chemical compound and disease context of BOLA

• Quinolone-photoconjugated major histocompatibility complex class II-binding peptides with lysine are antigenic for T cells mediating murine quinolone photoallergy [10].
• The induction of contact sensitivity in mice by hapten reagents such as trinitrochlorobenzene (TNCB) involves the activation of class II major histocompatibility complex (MHC)-restricted, hapten-specific, CD4+ T cells [11].
• Recombinant chimeric sequences originating from a mixture of the sequences of two different alleles are frequently found after amplification and cloning in Escherichia coli of exon 2 of the major histocompatibility complex (MHC) DRB genes [12].
• The effect of Escherichia coli lipopolysaccharide (LPS) on the expression of major histocompatibility complex (MHC) class II molecules by bovine mammary macrophages was examined [13].

Biological context of BOLA

• A possible explanation for the unique findings that the expression of anti-GPhe idiotypic determinants in mice of H-2q haplotype are dictated by the gene product in the MHC is that the macrophages in mice of H-2q haplotype present unique determinants of GPhe polymer in the response process to GHphe [14].
• Specific suppression of major histocompatibility complex class I and class II genes in astrocytes by brain-enriched gangliosides [15].
• Experiments were conducted to determine whether the acquisition of the secondary B cells' MHC collaborative phenotype was dependent on the presence of T cells during in vivo immunization [16].
• This induction is uniquely mediated by three DNA elements in the promoter region of class II MHC genes [17].
• These studies may be important for understanding mechanisms of central nervous system (CNS)-specific regulation of major histocompatibility molecules in neuroectodermal cells and the role of gangliosides in regulating MHC-restricted antiviral and autoimmune responses within the CNS [15].

Anatomical context of BOLA

• They also suggest that effector T lymphocytes can recognize antigen which is not associated with a major histocompatibility complex signal [18].
• In human B lymphoblastoid cell lines, the majority of major histocompatibility complex (MHC) class II heterodimers are located on the cell surface and in endocytic compartments, while invariant chain (Ii)-associated class II molecules represent biosynthetic intermediates which are present mostly in the endoplasmic reticulum and Golgi complex [19].
• The predominant peptides bound to major histocompatibility complex class II molecules expressed on human B cells are derived from a relatively limited number of self proteins [20].
• CD19+ peripheral blood B cells have fewer MIIC and surface MHC class II expression than DCs, while monocytes had low levels of MIIC and surface MHC class II [21].
• Major histocompatibility complex class II compartments in human B lymphoblastoid cells are distinct from early endosomes [19].

Associations of BOLA with chemical compounds

• We report here that both European and North American populations of moose (Alces alces) exhibit very low levels of genetic diversity at an expressed MHC class II DRB locus [22].
• Myelin/oligodendrocyte glycoprotein is a member of a subset of the immunoglobulin superfamily encoded within the major histocompatibility complex [23].
• Mapping of steroid 21-hydroxylase genes adjacent to complement component C4 genes in HLA, the major histocompatibility complex in man [24].
• Beta 1 interferon mRNA and beta interferon-inducible 2',5'-oligoadenylate synthetase mRNA were induced by growth under low-serum conditions in transformed BALB/c-3T3 cells, and antibodies to beta interferon blocked the induction of MHC class I antigen expression by serum deprivation in these cells [25].
• Observed influences of fixation and the addition of chloroquine or class II major histocompatibility complex-specific monoclonal antibodies on presenting function confirmed that ALVC process and present antigens using the endosomal pathway [26].

Regulatory relationships of BOLA

• Our studies show that IL-13 enhances proliferation and differentiation of bovine B cells and upregulates cell surface major histocompatibility complex (MHC) class II expression [27].
• PROBLEM: During the third trimester of pregnancy bovine trophoblast cells in the interplacentomal and arcade regions of the placenta express major histocompatibility complex class I (MHC-I) antigens [28].

Other interactions of BOLA

• The three-dimensional structure of beta 2-microglobulin, the light chain of the major histocompatibility complex class I antigens, has been determined by x-ray crystallography [29].
• The bovine major histocompatibility complex (BoLa): close linkage of the genes controlling serologically defined antigens and mixed lymphocyte reactivity [30].
• In humans, two of the inducible Hsp70 genes are located within the human major histocompatibility complex (MHC) on 6p21.3, as a duplicated locus, 12 kb apart from each other [31].
• This review focuses on recent advances in research on the bovine major histocompatibility complex (BoLA), with specific reference to the genetic organization, polymorphism and function of the class II genes [32].
• Analysis of cattle major histocompatibility complex (MHC) (BoLA) class I gene expression using serological and biochemical methods has demonstrated a high level of polymorphism [33].

Analytical, diagnostic and therapeutic context of BOLA

• We have now used immunoelectron microscopy and antigen presentation assays to compare freshly isolated DC (f-DC) and cultured DC (c-DC). f-DC display a round appearance, whereas c-DC display characteristic long processes. c-DC express much more cell surface major histocompatibility complex (MHC) class II than f-DC [21].
• Isoelectric focusing of bovine major histocompatibility complex class II molecules [34].
• Such acquisition occurred within 40 min of PMN coculture with isolated peripheral blood mononuclear cells, and this acquisition occurred with equal efficiency at 4 degrees C and 37 degrees C. The transfer of murine MHC class II to bovine PMNs precluded the possibility of endogenous protein expression [35].
• BACKGROUND: We have recently reported that interleukin (IL)-12 prevents acute graft-versus-host disease (GVHD)-induced mortality in a full major histocompatibility complex- plus multiple minor antigen-mismatched A/J-->B10 bone marrow transplantation (BMT) model [36].
• Analysis of the major histocompatibility complex in Syrian hamsters. I. Skin graft rejection, graft-versus-host reactions, mixed lymphocyte reactions, and immune response genes in inbred strains [37].

References