EVIDENCE THAT THE SAME GAMMA-DELTA T-CELLS RESPOND DURING INFECTION-INDUCED AND AUTOIMMUNE INFLAMMATION

Citation
A. Mukasa et al., EVIDENCE THAT THE SAME GAMMA-DELTA T-CELLS RESPOND DURING INFECTION-INDUCED AND AUTOIMMUNE INFLAMMATION, The Journal of immunology, 159(12), 1997, pp. 5787-5794
Citations number
44
Journal title
ISSN journal
00221767
Volume
159
Issue
12
Year of publication
1997
Pages
5787 - 5794
Database
ISI
SICI code
0022-1767(1997)159:12<5787:ETTSGT>2.0.ZU;2-4
Abstract
Inflammatory responses are induced in both testes of a mouse following injection of Listeria monocytogenes into one testis. Although the uni njected test is contains no detectable bacteria, it undergoes an autoi mmune attack. Normally, the testis lacks lymphocytes, but in the infec ted and autoimmune state, both gamma delta and alpha beta T cells are found as infiltrates. Here, we have examined the repertoire of the inf iltrating gamma delta T cells, using two different methods, and found a high frequency of V gamma 6/V delta 1 gamma delta T cells in both in fected and autoimmune testes. All of these expressed the invariant V g amma 6/V delta 1 TCR previously reported. However, secondary gamma and delta transcripts present within V gamma 6/V delta 1 hybridomas indic ated nonclonality. Interestingly, some of these secondary transcripts were derived from gamma gene rearrangements not previously found in th is gamma delta T cell subset, implying a difference in its origin. The increase in V gamma 6/V delta 1 cells observed here in both infected and autoimmune testes, together with our previous finding of a prefere ntial response by the same subset in Listeria-infected liver, indicate s that their response is triggered by the inflammation rather than by the infectious agent or because they are already resident in the tissu e. We and others have previously reported that the presence of gamma d elta T cells during certain inflammatory conditions correlates with le ss host tissue damage. This result, together with the evidence present ed here, further implies that a response by the V gamma 6/V delta 1 su bset in some way exerts a controlling influence on the host inflammato ry response.