| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
From the Unidad de Biología Experimental, Facultad de Medicina, UNAM, Apartado Postal 70343, México 20, D. F.; Department of Pediatrics and Microbiology and the Comprehensive Cancer Center, University of Alabama in Birmingham, Birmingham, Alabama; Departamento de Bioquímica, Centro de Investigación y de Estudios Avanzados del I.P.N., Apartado Postal 14-740, México 14, D. F.
Abstract
Paired immunofluorescent staining with antibodies specific for the major isotypes of mouse immunoglobulin was used to study the ontogenetic expression of diversity of cell surface immunoglobulin. The first B lymphocytes to emerge, derived from cytoplasmic IgM+ precursors, express sIgM exclusively. Between birth and 3 days of age separate populations of sIgM+ B lymphocytes acquire a second isotype: sIgD, one of the subclasses of sIgG, or sIgA. At 3 days, all splenic B lymphocytes that bear sIgG or sIgA also express sIgM, but virtually none stain for sIgD. By 7 days, a substantial proportion of sIgG+ or sIgA+ lymphocytes in spleen and most of those in lymph node express both sIgM and sIgD. Anti-µ antibody treatment from birth prevented development of B lymphocytes expressing any isotype. These observations suggest that the immature sIgM+ B lymphocyte is the pivotal cell in the generation of the different sublines of B cells and that sIgD is acquired as a third isotype on B lymphocytes already committed to eventual synthesis of IgG or IgA. The frequency of lymphocytes bearing only sIgG or sIgA is higher in old than in young mice, suggesting that sIgD and sIgM may be lost after stimulation by antigens. The occurrence of a nearly identical distribution of sIg isotypes on B lymphocytes from athymic, pathogen-free mice suggests that primary expression of isotype diversity does not require T cells.
Footnotes
1 This work was supported in part by Grants CA 16673 and CA 13148, awarded by the National Cancer Institute, and AI 11502, awarded by the National Institute of Allergy and Infectious Diseases, Department of Health, Education and Welfare.
2 Present address: Department of Zoology, University College, London, England.
3 Dr. Alexander R. Lawton is the recipient of a Research Career Development Award, AI 70780, from the National Institutes of Health.
4 On leave of absence from the National Institute for Medical Research, London, England. Correspondence should be addressed to Dr. R. M. E. Parkhouse, National Institute for Medical Research, The Ridgeway, Mill Hill, London, NW7 1AA, England.
This article has been cited by other articles:
|
|
 |
|
  R. A. Barrington, O. Pozdnyakova, M. R. Zafari, C. D. Benjamin, and M. C. Carroll B Lymphocyte Memory: Role of Stromal Cell Complement and Fc{gamma}RIIB Receptors J. Exp. Med., November 4, 2002; 196(9): 1189 - 1200. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. F. Ochsenbein, D. D. Pinschewer, S. Sierro, E. Horvath, H. Hengartner, and R. M. Zinkernagel Protective long-term antibody memory by antigen-driven and T help-dependent differentiation of long-lived memory B cells to short-lived plasma cells independent of secondary lymphoid organs PNAS, November 2, 2000; (2000) 230417497. [Abstract] [Full Text]
|
|
|
|
 |
|
 H. Igarashi and N. Sakaguchi Telomerase Activity Is Induced in Human Peripheral B Lymphocytes by the Stimulation to Antigen Receptor Blood, February 15, 1997; 89(4): 1299 - 1307. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. F. Ochsenbein, D. D. Pinschewer, S. Sierro, E. Horvath, H. Hengartner, and R. M. Zinkernagel Protective long-term antibody memory by antigen-driven and T help-dependent differentiation of long-lived memory B cells to short-lived plasma cells independent of secondary lymphoid organs PNAS, November 21, 2000; 97(24): 13263 - 13268. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
