Dynamics of memory T cell proliferation under conditions of heterologous immunity and bystander stimulation

被引:77
作者
Kim, SK [1 ]
Brehm, MA [1 ]
Welsh, RM [1 ]
Selin, LK [1 ]
机构
[1] Univ Massachusetts, Dept Pathol, Worcester, MA 01655 USA
关键词
D O I
10.4049/jimmunol.169.1.90
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
By examining adoptively transferred CSFE-labeled lymphocytic choriomeningitis virus (LCMV)-immune donor T cells in Thy-1 congenic hosts inoculated with viruses or with the cytokine inducer poly(I:Q, strikingly different responses of bona fide memory T cells were found in response to different stimuli. Poly(I:Q (cytokine) stimulation caused a limited synchronized division of memory CD8 T cells specific to each of five LCMV epitopes, with no increase and sometimes a loss in number, and no change in their epitope hierarchy. Homologous LCMV infection caused more than seven divisions of T cells specific for each epitope, with dramatic increases in number and minor changes in hierarchy. Infections with the heterologous viruses Pichinde and vaccinia (VV) caused more than seven divisions and increases in number of T cells specific to some putatively cross-reactive but not other epitopes and resulted in substantial changes in the hierarchy of the LCMV-specific T cells. Hence, there can be memory T cell division without proliferation (i.e., increase in cell number) in the absence of Ag and division with proliferation in the presence of Ag from homologous or heterologous viruses. Heterologous protective immunity between viruses is not necessarily reciprocal, given that LCMV protects against VV but VV does not protect against LCMV. VV elicited proliferation of LCMV-induced CD8 and CD4 T cells, whereas LCMV did not elicit proliferation of VV-induced T cells. Thus, depending on the pathogen and the sequence of infection, a heterologous agent may selectively stimulate the memory pool in patterns consistent with heterologous immunity.
引用
收藏
页码:90 / 98
页数:9
相关论文
共 37 条
[1]   Evolution of the T cell repertoire during primary, memory, and recall responses to viral infection [J].
Blattman, JN ;
Sourdive, DJD ;
Murali-Krishna, K ;
Ahmed, R ;
Altman, JD .
JOURNAL OF IMMUNOLOGY, 2000, 165 (11) :6081-6090
[2]  
BREHM MA, IN PRESS NAT IMMUNOL
[3]   Memory CD8+T cells in heterologous antiviral immunity and immunopathology in the lung [J].
Chen, HD ;
Fraire, AE ;
Joris, I ;
Brehm, MA ;
Welsh, RM ;
Selin, LK .
NATURE IMMUNOLOGY, 2001, 2 (11) :1067-1076
[4]   Virus subversion of immunity: a structural perspective [J].
Gewurz, BE ;
Gaudet, R ;
Tortorella, D ;
Wang, EW ;
Ploegh, HL .
CURRENT OPINION IN IMMUNOLOGY, 2001, 13 (04) :442-450
[5]  
Gudmundsdottir H, 1999, J IMMUNOL, V162, P5212
[6]   Recombinant vaccinia virus-induced T-cell immunity: Quantitation of the response to the virus vector and the foreign epitope [J].
Harrington, LE ;
van der Most, R ;
Whitton, JL ;
Ahmed, R .
JOURNAL OF VIROLOGY, 2002, 76 (07) :3329-3337
[7]   Memory CD8+ T cell differentiation:: initial antigen encounter triggers a developmental program in naive cells [J].
Kaech, SM ;
Ahmed, R .
NATURE IMMUNOLOGY, 2001, 2 (05) :415-422
[8]  
KOS FJ, 1993, J IMMUNOL, V150, P387
[9]   Stability and diversity of T cell receptor repertoire usage during lymphocytic choriomeningitis virus infection of mice [J].
Lin, MY ;
Welsh, RM .
JOURNAL OF EXPERIMENTAL MEDICINE, 1998, 188 (11) :1993-2005
[10]   Viral immune evasion strategies and the underlying cell biology [J].
Lorenzo, ME ;
Ploegh, HL ;
Tirabassi, RS .
SEMINARS IN IMMUNOLOGY, 2001, 13 (01) :1-9