Journal article
B-1 Cells in Systemic Autoimmune Responses: IGM+, FCϵRDULL B Cells Are Lost During Chronic Graft-Versus-Host Disease But Not in Murine AIDS or Collagen-Induced Arthritis
Immunological investigations, Vol.23(4-5), pp.293-311
01/01/1994
DOI: 10.3109/08820139409066825
PMID: 7525472
Abstract
The potential role of B-1 cells (i.e the CD5
+
B cell and "sister" B cell subsets) in autoimmunity is controversial. CD5
+
B cells have been shown to secrete antibodies of similar specificity as those found in many systemic autoimmune diseases; in addition, increases in CD5
+
B cell frequency have been reported in patients suffering from rheumatoid arthritis, Sjögren's syndrome, myasthenia gravis, insulin-dependent diabetes mellitus and Hashimoto's thyroiditis. Whether these increases are due to expansion of B-1 lineage cells in the human or due to activation-induced expression of CD5 by conventional B cells is unclear. In the present study, we used three murine models of systemic autoimmunity: murine acquired immunodeficiency syndrome (MAIDS), chronic graft-versus-host disease (cGvHD), and collagen-induced arthritis (CIA) to determine whether increases in B-1 cell frequency are universally seen in models of autoimmunity which are mechanistically distinct. In contrast to the aforementioned human systemic autoimmune diseases which exhibit an increase in CD5
+
B cell frequency, the percentage of CD5
+
B cells declined in all three murine models of systemic autoimmune disease. Even though there was a decrease in the frequency of CD5
+
B cells there was no change in the actual number of CD5
+
B cells. Thus, the apparent decline in CD5
+
B cell frequency was due to increases in either T cells, conventional FcR
+
B cells, or both. The only actual decline in a B cell subset was the loss of IgM
+
, Fc±R
dull
cells in both the spleen and peritoneal cavity of mice undergoing a chronic graft-versus-host reaction. Therefore, our data suggests that expansion of the B-1 subset does not occur as a general feature of murine systemic autoimmune disease. These observations, consistent with previous studies of Ig gene usage in autoreactive antibodies, support the view that expansion and differentiation of the CD5
+
B cell subset is not a central event leading to autoantibody production.
Details
- Title: Subtitle
- B-1 Cells in Systemic Autoimmune Responses: IGM+, FCϵRDULL B Cells Are Lost During Chronic Graft-Versus-Host Disease But Not in Murine AIDS or Collagen-Induced Arthritis
- Creators
- Laurie A IciekThomas J WaldschmidtMarie M GriffithsKathryn H Brooks
- Resource Type
- Journal article
- Publication Details
- Immunological investigations, Vol.23(4-5), pp.293-311
- Publisher
- Taylor & Francis
- DOI
- 10.3109/08820139409066825
- PMID
- 7525472
- ISSN
- 0882-0139
- eISSN
- 1532-4311
- Language
- English
- Date published
- 01/01/1994
- Academic Unit
- Pathology
- Record Identifier
- 9984047682502771
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