IgE Allotypes in Sera of Mice with Autoimmune Diseases and in Mice with Graft-versus-Host Disease after Transfusion or Bone Marrow Transplantation

Abstract

Isotype- and allotype-specifíc IgE determinations by sandwich ELISA with monoclonal antibodies to Igh-7 (6HD5, HMK-12), Igh-7^a (No. 297) and Igh-7^b/JKS-6) were used to qualitate antibodies of the IgE class. The sensitivity of the method is 0.1 ng/ml. Serum IgE levels were much higher in mice infected with Nippostrongylus brasiliensis. In sera of BALB/c, AKR and C3H/JCL mice only IgE^a, in sera of C57BL/6 and CB-20 only IgE^b, in sera of (BALB/c × C57BL/6) F1 mice, both allotypes were detected, as expected. In mice with autoimmune diseases, such as NZB, NZW, (NZB × NZW) F1, MRL/Ipr and MRL/n strains which all belong to the IgE^a allotype group, IgE and IgE^a were very high. In the sera of BXSB mice, both IgE^a and IgE^b were detected. Both IgE^a and IgE^b from donor and host were increased in the sera of mice with graft-versus-host disease after transplantation but only the IgE^a (from the donor) was increased in mice with graft-versus-host disease after bone marrow transplantation. In the former, both B cells (from donor and host) secreted IgE, whereas in the latter only the donor cells did. These are the first observations showing the importance of IgE allotype secretion as an indication of graf-versus-host disease.

The FcRβ- and γ-ITAMs Play Crucial but Distinct Roles in the Full Activation of Mast Cells Induced by IgEκ and Protein L

“…In this study, the murine IgEk clones that were examined, with the exception of 15.3.2, showed little or no binding to PpL, which was similar to the previous finding that out of six murine IgGk clones, at least three could not bind to PpL (34). Murine IgE clones have been divided into two allotypes, IgE a and IgE b (35). Because 15.3.2, 27.74, and H1-ε-26.82 are IgE a allotypes, and C48-2 is an IgE b allotype, we believe that the specific IgE allotype does not determine the ability of IgEk to bind to PpL.…”

Basophils and the T helper 2 environment can promote the development of lupus nephritis

“…Some mouse models of spontaneous SLE, like BXSB and MRL- Fas lpr show increases in the T H 1 cytokine IFN-γ as linked to the expression of the T H 1 mediated isotypes, IgG2a and IgG3, and deletion of the IFN-γ gene in the context of these backgrounds was shown to eliminate disease4,49. Nonetheless, it is less well known that many of the spontaneous mouse models ( NZB , NZW , BXSB , and MRL / Fas lpr ) of lupus-like disease have high circulating levels of IgE52, suggesting the possibility of a contributory role for a T H 2 component in these models. SLE patients showed both T H 1 and T H 2 responses and both IgG-CIC's and IgE-CIC's were associated with increased disease activity.…”

Natural IgE Production in the Absence of MHC Class II Cognate Help

“…For detection of anti-PC IgE, total IgE was captured with anti-IgE (clone 6HD5) and anti-PC-specific IgE was detected by addition of PC-BSA (50 mg/ml) followed by an HRP-labeled anti-PC Ab. For detection of allotype-specific IgE, total IgE was captured with anti-IgE b (clone JKS-6) or anti-IgE a (clone UH297) and detected with an HRP-labeled anti-IgE (clone HMK-12) (Miyajima et al, 1996). For detection of anti-idiotypic IgE, total IgE was captured with anti-IgE (clone 6HD5) and idiotypic IgE detected with biotin-conjugated anti-KL25 (clone IIIC4) or anti-VI10 (clone 35.61) idiotypic antibodies and HRP-conjugated streptavidin (Hangartner et al, 2003).…”