Disease relevance of Ea1

• An antigen-specific factor capable of augmenting delayed-type hypersensitivity (DH) in the culture supernatants from immune spleen cells and erythrocyte antigen has been found [1].
• To elucidate whether this kind of factor (DTH-augmentation factor; DAF) participates in the establishment of DTH to various kinds of antigen besides erythrocyte antigen, we chose a bacterial antigen, Listeria monocytogenes, which is a facultative intracellular bacterium [2].

High impact information on Ea1

• The results indicate that TH cells possess genetically restricted receptors for macrophage I-J-subregion gene products and that the interaction between this receptor and the macrophage I-J-subregion determinants is essential for the initiation of a primary in vitro antibody response to an erythrocyte antigen [3].
• Neither Ea1 nor Ea2 are restricted to lymphocytes [4].
• This pattern of reactivity among fifteen H-2 haplotypes is unlike the strain distribution for any known H-2 erythrocyte antigen, and is exactly antithetical to the S region-controlled H-2.7 antigen [5].
• These 15A-associated Ids are expressed by some heterologous human antimeningococcal B polysaccharide MAbs, and they also are independently expressed by two human MAbs that are specific for either the H. influenzae b polysaccharide or the i erythrocyte antigen and that utilize the kappa I-15A V region [6].
• Murine erythrocyte antigen H-2.7(G): expression depends on level of complement component C4 [7].

Biological context of Ea1

• Active immunity to a xenogeneic erythrocyte antigen is potentiated by pregnancy [8].

Anatomical context of Ea1

• CSA blocks at a point before the biosynthesis of Ea1 and after that of T3/T cell receptor loss from the cell surface, at a point close to Ea2 biosynthesis [4].
• We previously found an antigen-specific factor capable of augmenting delayed-type hypersensitivity (DTH) in the culture supernatant of the mixture of immune spleen cells and erythrocyte antigen, or in the serum of mice immunized with heterologous erythrocytes and exhibiting delayed-type footpad reaction [2].
• Mice treated with inhibitors of prostaglandin synthetase showed an alteration in the number of spontaneous, anti-autologous erythrocyte antigen (Hb)-antibody-forming cells in the spleens [9].
• Oral immunization of erythrocyte antigen induces antigen-specific Tcs cells in Peyer's patches which predominantly support IgA responses with minor IgM and IgG responses upon adoptive transfer to tolerized mice [10].

Associations of Ea1 with chemical compounds

• Monoclonal antibody-specific immobilization of erythrocyte antigen analysis with anti-VLAN and with several mouse monoclonal antibodies directed at epitopes on the Kell glycoprotein gave positive results, indicating that the VLAN antigen is located on the Kell glycoprotein [11].

Analytical, diagnostic and therapeutic context of Ea1

• An immunoradiometric assay has been used to determine the rate of loss of host erythrocyte antigen from the tegumental surface of adult Schistosoma mansoni [12].

References