Bcmd governs recruitment of newly formed B-2 cells into the stable peripheral B cell pool.

Format:

Book

Thesis/Dissertation

Author/Creator:

Lentz, Vicky Mischel.

Contributor:

University of Pennsylvania.

Language:

English

Subjects (All):

Immunology.

Cytology.

Molecular biology.

0307.

0379.

0982.

Penn dissertations--Immunology.

Immunology--Penn dissertations.

Local Subjects:

Penn dissertations--Immunology.

Immunology--Penn dissertations.

0307.

0379.

0982.

Physical Description:

106 pages

Contained In:

Dissertation Abstracts International 58-07B.

System Details:

Mode of access: World Wide Web.

text file

Summary:

The A/WySnJ strain of mice harbors a single autosomal trait that causes profound B cell deficiency. The studies described herein further characterize Bcmd, and provide insight regarding the mechanisms involved in recruitment of cells to the long lived peripheral B cell pool. The results of cytofluorimetric and BrdU labeling studies show that Bcmd reduces peripheral B cell life span. In addition, reciprocal and mixed bone marrow chimeras were constructed, and demonstrate that Bcmd is an intrinsic B cell defect. Further, cytofluorimetric analysis coupled with in vitro TUNEL assays show that Bcmd results in an increased apoptotic death rate among peripheral B cells, suggesting it interferes with signals that normally avert programmed cell death. Finally, cytofluorimetric and BrdU labeling analyses of B-1 cells reveal they are unaffected by Bcmd, indicating that B-1 and B-2 cells differ in their requisites for maturation and longevity. These studies suggest that discrete events which mediate recruitment of transitional B cells into the long lived pool occur during late stages of peripheral B cell maturation. Further, they suggest that in the absence of these events, the default pathway is programmed cell death. Finally, since the shortened life span of mature A/WySnJ B cells affects neither primary humoral responses, initiation of germinal centers nor isotype switching, at least one determinant of B cell longevity is separable from antigen-driven processes.

Notes:

Thesis (Ph.D. in Immunology) -- University of Pennsylvania, 1997.

Source: Dissertation Abstracts International, Volume: 58-07, Section: B, page: 3545.

Local Notes:

School code: 0175.

ISBN:

9780591502091

Access Restriction:

Restricted for use by site license.