Journal article
The regulation of the expression of gp39, the CD40 ligand, on normal and cloned CD4+ T cells
The Journal of immunology (1950), Vol.151(5), pp.2497-2510
1993
DOI: 10.4049/jimmunol.151.5.2497
PMID: 8103067
Abstract
Studies have established that gp39, the ligand for CD40, induces B cell cycle entry and is involved in the initiation of the humoral immune response. Expression of gp39 has been observed on normal, activated CD4+ T cells, activated lymph node cells; an activated Th1 clone, and an activated Th2 clone. Anti-CD3-activated CD8+ T cells did not express gp39; however, CD8+ T cells activated with PMA/ionomycin expressed gp39. The kinetics of anti-CD3-induced gp39 expression on a T cell clone and on splenic CD4+ T cells showed that gp39 was detectable at 4 h after activation, reaching maximal levels between 6 to 8 h postactivation and returning to near resting levels between 24 to 48 h. Lymphokines modulated the expression of gp39 on activated T cells. Expression of gp39 was inhibited by IFN-gamma on activated Th1, Th2, and CD4+ T cells; whereas TGF-beta inhibited gp39 expression only on the Th2 clone studied. All other lymphokines tested were without substantial effect. Differences in the expression of gp39 on activated naive and memory T cells were observed, as well as differences in requirements for optimal gp39 expression on these subsets. There are correlations between gp39 expression and effector function; however, anti-CD3-activated splenic CD4+ cells that express gp39 did not exhibit effector function. A comparison of the relative numbers of molecules of gp39 shows that activated Th1 clones express at least 20-fold the number of gp39 molecules/cell compared with activated splenic CD4+ cells. This may imply that density of gp39 on the activated T cells plays an important role in determining effector function.
Details
- Title: Subtitle
- The regulation of the expression of gp39, the CD40 ligand, on normal and cloned CD4+ T cells
- Creators
- Meenakshi Roy - Dartmouth medical school, dep. microbiology, Lebanon NH 03756, United StatesThomas Waldschmidt - Dartmouth medical school, dep. microbiology, Lebanon NH 03756, United StatesAlejandro Aruffo - Dartmouth medical school, dep. microbiology, Lebanon NH 03756, United StatesJeffrey A Ledbetter - Dartmouth medical school, dep. microbiology, Lebanon NH 03756, United StatesRandolph J Noelle - Dartmouth medical school, dep. microbiology, Lebanon NH 03756, United States
- Resource Type
- Journal article
- Publication Details
- The Journal of immunology (1950), Vol.151(5), pp.2497-2510
- DOI
- 10.4049/jimmunol.151.5.2497
- PMID
- 8103067
- NLM abbreviation
- J Immunol
- ISSN
- 0022-1767
- eISSN
- 1550-6606
- Publisher
- American Association of Immunologists; Bethesda, MD
- Language
- English
- Date published
- 1993
- Academic Unit
- Pathology
- Record Identifier
- 9984047790702771
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