The JI
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     
 


This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Raveche, E. S.
Right arrow Articles by Conroy, J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Raveche, E. S.
Right arrow Articles by Conroy, J.

The Journal of Immunology, Vol 141, Issue 12 4133-4139, Copyright © 1988 by American Association of Immunologists


ARTICLES

In vivo effects of hyperdiploid Ly-1+ B cells of NZB origin

ES Raveche, P Lalor, A Stall and J Conroy
Department of Microbiology and Immunology, Albany Medical College, NY 12208.

Cells with increased chromosome number and DNA content have been found in the spleens of old NZB mice. These hyperdiploid cells are of clonal origin and demonstrate discrete IgH chain gene rearrangements by Southern blot analysis. In this report, hyperdiploid cells were analyzed by three-color flow cytometric techniques and found to be Ly- 1+ B cells which were dull for Ly-1 and bright for surface IgM. These cells, unlike typical diploid Ly-1+ B cells, were negative for B220/6B2 and surface IgD. Hyperdiploid Ly-1+ B cells were found to be the predominant splenic subpopulation in animals receiving a spleen cell transfer from donors which possessed hyperdiploid Ly-1+ B cells. (NZB x DBA/2)F1 recipients of NZB spleen cells demonstrated a 10- to 1000-fold increase in Ly-1+ B cells in the spleen but showed no increased levels of Ly-1+ B cells in the peritoneum. Nearly all the splenic Ly-1+ B cells were hyperdiploid with the phenotype of the NZB parent. Cytogenetic analysis revealed that all the hyperdiploid cells were NZB donor cells. These findings suggest that the increase in splenic Ly-1+ B cells in the F1 recipients was due to expansion of injected splenic hyperdiploid Ly-1+ B cells of NZB origin. All of the F1 recipients of NZB hyperdiploid Ly-1+ B cells demonstrated a significant decrease in endogenous B cells as well as decreased serum IgM and anti-ssDNA autoantibodies. These studies suggest that hyperdiploid Ly-1+ B cells are different from typical peritoneal Ly-1+ B cells both in the lymphoid organs to which they home and in their proliferative capacity. NZB hyperdiploid Ly-1+ B cells, which may arise as a natural consequence of hyperactive Ly-1+ B cells, may play an immunoregulatory role in the spleen.


This article has been cited by other articles:


Home page
BloodHome page
E. S. Raveche, E. Salerno, B. J. Scaglione, V. Manohar, F. Abbasi, Y.-C. Lin, T. Fredrickson, P. Landgraf, S. Ramachandra, K. Huppi, et al.
Abnormal microRNA-16 locus with synteny to human 13q14 linked to CLL in NZB mice
Blood, June 15, 2007; 109(12): 5079 - 5086.
[Abstract] [Full Text] [PDF]


Home page
J. Immunol.Home page
C. Haas, B. Ryffel, and M. Le Hir
IFN-{gamma} Receptor Deletion Prevents Autoantibody Production and Glomerulonephritis in Lupus-Prone (NZB NZW)F1 Mice
J. Immunol., April 15, 1998; 160(8): 3713 - 3718.
[Abstract] [Full Text] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
This Website Copyright © 1988 by The American Association of Immunologists, Inc. All rights reserved.
All Contents Copyright © 1988 by The American Association of Immunologists, Inc. All rights reserved.