Abstract
Abnormal expansion of autoantibody-synthesizing B cells and self-reactive T cells, which most likely escape negative selection within the thymus, have both been characterized and reasoned to play a role in the pathogenesis of autoimmunity in NZB mice. Support for this thesis has been our observation that NZB mice have severe cortical and medullary thymic microarchitectural defects. As a means to dissect the roles of T and B cells in the induction of such abnormalities, B cell-deficient NZB mice were bred by backcrossing the Igh6null allele on to the NZB background (NZB-μMT mice). Such mice showed undetectable levels of autoantibodies. NZB-μMT mice, as compared to wild-type NZB mice, had lower absolute numbers of CD4+ T cells. Furthermore, thymic abnormalities in NZB-μMT mice were restricted to the medulla. These data suggest that, while B cells may play a role in thymic cortical abnormalities, the medullary abnormalities are induced by other mechanisms.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 393-400 |
| Number of pages | 8 |
| Journal | Journal of Autoimmunity |
| Volume | 16 |
| Issue number | 4 |
| DOIs | |
| State | Published - 2001 |
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Keywords
- Autoimmunity
- B lymphocytes
- Rodent
- Stromal cells
ASJC Scopus subject areas
- Immunology
- Immunology and Allergy
Cite this
B cells are selectively associated with thymic cortical but not medullary pathology in NZB mice. / Taguchi, Nobuyoshi; Hashimoto, Yoshiko; Hsu, Tom; Ansari, Aftab A.; Shultz, Len; Dorshkind, Kenneth; Ikehara, Susumu; Naiki, Mitsuru; Gershwin, M. Eric.
In: Journal of Autoimmunity, Vol. 16, No. 4, 2001, p. 393-400.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - B cells are selectively associated with thymic cortical but not medullary pathology in NZB mice
AU - Taguchi, Nobuyoshi
AU - Hashimoto, Yoshiko
AU - Hsu, Tom
AU - Ansari, Aftab A.
AU - Shultz, Len
AU - Dorshkind, Kenneth
AU - Ikehara, Susumu
AU - Naiki, Mitsuru
AU - Gershwin, M. Eric
PY - 2001
Y1 - 2001
N2 - Abnormal expansion of autoantibody-synthesizing B cells and self-reactive T cells, which most likely escape negative selection within the thymus, have both been characterized and reasoned to play a role in the pathogenesis of autoimmunity in NZB mice. Support for this thesis has been our observation that NZB mice have severe cortical and medullary thymic microarchitectural defects. As a means to dissect the roles of T and B cells in the induction of such abnormalities, B cell-deficient NZB mice were bred by backcrossing the Igh6null allele on to the NZB background (NZB-μMT mice). Such mice showed undetectable levels of autoantibodies. NZB-μMT mice, as compared to wild-type NZB mice, had lower absolute numbers of CD4+ T cells. Furthermore, thymic abnormalities in NZB-μMT mice were restricted to the medulla. These data suggest that, while B cells may play a role in thymic cortical abnormalities, the medullary abnormalities are induced by other mechanisms.
AB - Abnormal expansion of autoantibody-synthesizing B cells and self-reactive T cells, which most likely escape negative selection within the thymus, have both been characterized and reasoned to play a role in the pathogenesis of autoimmunity in NZB mice. Support for this thesis has been our observation that NZB mice have severe cortical and medullary thymic microarchitectural defects. As a means to dissect the roles of T and B cells in the induction of such abnormalities, B cell-deficient NZB mice were bred by backcrossing the Igh6null allele on to the NZB background (NZB-μMT mice). Such mice showed undetectable levels of autoantibodies. NZB-μMT mice, as compared to wild-type NZB mice, had lower absolute numbers of CD4+ T cells. Furthermore, thymic abnormalities in NZB-μMT mice were restricted to the medulla. These data suggest that, while B cells may play a role in thymic cortical abnormalities, the medullary abnormalities are induced by other mechanisms.
KW - Autoimmunity
KW - B lymphocytes
KW - Rodent
KW - Stromal cells
UR - http://www.scopus.com/inward/record.url?scp=0034948562&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0034948562&partnerID=8YFLogxK
U2 - 10.1006/jaut.2001.0515
DO - 10.1006/jaut.2001.0515
M3 - Article
C2 - 11437487
AN - SCOPUS:0034948562
VL - 16
SP - 393
EP - 400
JO - Journal of Autoimmunity
JF - Journal of Autoimmunity
SN - 0896-8411
IS - 4
ER -