CD4-CD8- T cells control intracellular bacterial infections both in vitro and in vivo

被引:105
作者
Cowley, SC
Hamilton, E
Frelinger, JA
Su, J
Forman, J
Elkins, KL [1 ]
机构
[1] US FDA, Ctr Biol Evaluat & Res, Lab Mycobacterial Dis & Cellular Immunol, Rockville, MD 20852 USA
[2] Univ N Carolina, Dept Microbiol & Immunol, Chapel Hill, NC 27599 USA
[3] Univ Texas, SW Med Ctr, Ctr Immunol, Dallas, TX 75390 USA
关键词
D O I
10.1084/jem.20050569
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Memory T cells, including the well-known CD4(+) and CD8(+) T cells, are central components of the acquired immune system and are the basis for successful vaccination. After infection, CD4(+) and CD8(+) T cells expand into effector cells, and then differentiate into long- lived memory cells. We show that a rare population of CD4(-)CD8(-)CD3(+)alpha beta(+)gamma delta(-)NK1.1(-) T cells has similar functions. These cells potently and specifically inhibit the growth of the intracellular bacteria Mycobacterium tuberculosis ( M. tb.) or Francisella tularensis Live Vaccine Strain ( LVS) in macrophages in vitro, promote survival of mice infected with these organisms in vivo, and adoptively transfer immunity to F. tularensis LVS. Furthermore, these cells expand in the spleens of mice infected with M. tb. or F. tularensis LVS, and then acquire a memory cell phenotype. Thus, CD4(-)CD8(-) T cells have a role in the control of intracellular infection and may contribute to successful vaccination.
引用
收藏
页码:309 / 319
页数:11
相关论文
共 48 条
[1]   Absence of programmed death receptor 1 alters thymic development and enhances generation of CD4/CD8 double-negative TCR-transgenic T cells [J].
Blank, C ;
Brown, I ;
Marks, R ;
Nishimura, H ;
Honjo, T ;
Gajewski, TF .
JOURNAL OF IMMUNOLOGY, 2003, 171 (09) :4574-4581
[2]   Susceptibility to secondary Francisella tularensis live vaccine strain infection in B-cell-deficient mice is associated with neutrophilia but not with defects in specific T-cell-mediated immunity [J].
Bosio, CM ;
Elkins, KL .
INFECTION AND IMMUNITY, 2001, 69 (01) :194-203
[3]   THE ORIGIN OF CD4(-)CD8(-)TCR-ALPHA-BETA(+) THYMOCYTES - A MODEL-BASED ON T-CELL RECEPTOR AVIDITY [J].
BUDD, RC ;
MIXTER, PF .
IMMUNOLOGY TODAY, 1995, 16 (09) :428-431
[4]   Expansion of TcRαβ+CD3+CD4-CD8-(CD4/CD8 double-negative) T lymphocytes in a case of staphylococcal toxic shock syndrome [J].
Carulli, G ;
Lagomarsini, G ;
Azzarà, A ;
Testi, R ;
Riccioni, R ;
Petrini, M .
ACTA HAEMATOLOGICA, 2004, 111 (03) :163-167
[5]   LPR AND GLD - SINGLE GENE MODELS OF SYSTEMIC AUTOIMMUNITY AND LYMPHOPROLIFERATIVE DISEASE [J].
COHEN, PL ;
EISENBERG, RA .
ANNUAL REVIEW OF IMMUNOLOGY, 1991, 9 :243-269
[6]   CD4(+) AND CD8(+) T-CELL-DEPENDENT AND T-CELL-INDEPENDENT HOST-DEFENSE MECHANISMS CAN OPERATE TO CONTROL AND RESOLVE PRIMARY AND SECONDARY FRANCISELLA-TULARENSIS LVS INFECTION IN MICE [J].
CONLAN, JW ;
SJOSTEDT, A ;
NORTH, RJ .
INFECTION AND IMMUNITY, 1994, 62 (12) :5603-5607
[7]   CD4+ T cells mediate IFN-γ-independent control of Mycobacterium tuberculosis infection both in vitro and in vivo [J].
Cowley, SC ;
Elkins, KL .
JOURNAL OF IMMUNOLOGY, 2003, 171 (09) :4689-4699
[8]   Multiple T cell subsets control Francisella tularensis LVS intracellular growth without stimulation through macrophage interferon γ receptors [J].
Cowley, SC ;
Elkins, KL .
JOURNAL OF EXPERIMENTAL MEDICINE, 2003, 198 (03) :379-389
[9]  
Culkin SJ, 1997, J IMMUNOL, V158, P3277
[10]   Tularemia as a biological weapon - Medical and public health management [J].
Dennis, DT ;
Inglesby, TV ;
Henderson, DA ;
Bartlett, JG ;
Ascher, MS ;
Eitzen, E ;
Fine, AD ;
Friedlander, AM ;
Hauer, J ;
Layton, M ;
Lillibridge, SR ;
McDade, JE ;
Osterholm, MT ;
O'Toole, T ;
Parker, G ;
Perl, TM ;
Russell, PK ;
Tonat, K .
JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION, 2001, 285 (21) :2763-2773