PMID- 3123558 OWN - NLM STAT- MEDLINE DCOM- 19880315 LR - 20201214 IS - 0022-202X (Print) IS - 0022-202X (Linking) VI - 90 IP - 2 DP - 1988 Feb TI - Immunoglobulin class and subclass profile of the Ro/SS-A autoantibody response. PG - 158-64 AB - We have developed an enzyme-linked immunosorbent assay (ELISA) for autoantibody to Ro/SS-A antigen (anti-Ro/SS-A) in order to more fully characterize the autoimmune response that occurs to this antigen in patients with subacute cutaneous lupus erythematosus (SCLE). The microtiter plate-immobilized, biochemically purified Ro/SS-A antigen reacted with anti-Ro/SS-A antibody, but not with other closely related specificities (anti-La/SS-B, anti-SM, anti-U1-RNP) or normal sera. The optimal pH of antigen-antibody reaction in this ELISA was 7.2. The binding of sera containing anti-Ro/SS-A was inhibited 80% by preincubation with the same amount of Ro/SS-A antigen used for coating the plate. Although 11 of the 14 (79%) SCLE sera studied had precipitating anti-Ro/SS-A antibody by immunodiffusion, 13 (93%) sera had abnormally elevated IgG, IgA, or IgM ELISA binding levels. A good correlation between IgG anti-Ro/SS-A ELISA binding levels and immunodiffusion titers was observed (r - 0.8588, p less than or equal to 0.001) suggesting that IgG is the major anti-Ro/SS-A antibody class detected by double immunodiffusion, Sera with a combination of high rheumatoid factor levels (latex 3+ or higher) and high anti-Ro/SS-A titers (1:8 or higher in immunodiffusion) tended to give an abnormally high IgM anti-Ro/SS-A ELISA binding levels. After rheumatoid factor activity was removed by absorption with heat-aggregated human IgG, a 50% decrease in IgM anti-Ro/SS-A ELISA binding was noted. On the other hand, absorption of rheumatoid factor-negative sera that contained high IgM anti-Ro/SS-A binding activity did not significantly decrease ELISA binding levels. Prednisone and 6-azathioprine reduced the level of IgG anti-Ro/SS-A autoantibody in sera of treated SCLE patients by 50%. The IgG subclass profile of anti-Ro/SS-A autoantibody was analyzed by using mouse monoclonal antibodies specific for the 4 human IgG subclasses. Of anti-Ro/SS-A positive SCLE sera, 91% had predominantly IgG1 subclass autoantibody. The coexistence of IgM and IgG anti-Ro/SS-A autoantibody and the predominance of the IgG1 subclass is compatible with the possibility that this autoantibody response is under T-cell control. The predominance of IgG1 in the autoimmune response to Ro/SS-A antigen in SCLE patients is consistent with the hypothesis that antibody dependent cell mediated cytotoxicity could be an important immunologic effector mechanism in this disorder. FAU - Lieu, T S AU - Lieu TS AD - Department of Dermatology, University of Texas Health Science Center, Dallas 75235. FAU - Reimer, C B AU - Reimer CB FAU - Sontheimer, R D AU - Sontheimer RD LA - eng GR - AM19101/AM/NIADDK NIH HHS/United States PT - Journal Article PT - Research Support, Non-U.S. Gov't PT - Research Support, U.S. Gov't, P.H.S. PL - United States TA - J Invest Dermatol JT - The Journal of investigative dermatology JID - 0426720 RN - 0 (Autoantibodies) RN - 0 (Autoantigens) RN - 0 (Immunoglobulin G) RN - 0 (Immunoglobulin M) RN - 0 (Immunosuppressive Agents) RN - 0 (RNA, Small Cytoplasmic) RN - 0 (RO60 protein, human) RN - 0 (Ribonucleoproteins) RN - 0 (SS-A antigen) RN - 9009-79-4 (Rheumatoid Factor) SB - IM MH - Animals MH - Autoantibodies/*analysis/classification MH - Autoantigens/*immunology MH - Enzyme-Linked Immunosorbent Assay MH - Humans MH - Hydrogen-Ion Concentration MH - Immunodiffusion MH - Immunoglobulin G/*analysis/classification MH - Immunoglobulin M/*analysis/classification MH - Immunosuppressive Agents/pharmacology MH - Lupus Erythematosus, Cutaneous/immunology MH - Mice MH - *RNA, Small Cytoplasmic MH - Rheumatoid Factor/analysis MH - *Ribonucleoproteins EDAT- 1988/02/01 00:00 MHDA- 1988/02/01 00:01 CRDT- 1988/02/01 00:00 PHST- 1988/02/01 00:00 [pubmed] PHST- 1988/02/01 00:01 [medline] PHST- 1988/02/01 00:00 [entrez] AID - S0022-202X(88)91136-0 [pii] AID - 10.1111/1523-1747.ep12462142 [doi] PST - ppublish SO - J Invest Dermatol. 1988 Feb;90(2):158-64. doi: 10.1111/1523-1747.ep12462142.