Home LiteratureArticle Details
PMID: 10760288 Published · ppublish English Journal Article Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, P.H.S.

Relative contributions of distinct MHC class I-dependent cell populations in protection to tuberculosis infection in mice.

Proceedings of the National Academy of Sciences of the United States of America ·Vol. 97 ·No. 8 ·2000-04-11 ·Pages 4204-8

Sousa AO, Mazzaccaro RJ, Russell RG, Lee FK, Turner OC, Hong S, Van Kaer L, Bloom BR

Abstract

A necessary role for cytotoxic T lymphocytes in protection against Mycobacterium tuberculosis (MTB) has been suggested by studies of the beta2-microglobulin-deficient mouse, which is unable to present antigens through MHC class I and class I-like molecules and invariably succumbs early after infection. To identify the relative contributions of distinct putative MHC class I-dependent cell populations in protection against tuberculosis, we compared a variety of gene-disrupted mouse strains for susceptibility to MTB infection. Among the strains tested, the most susceptible mice, as measured by survival time and bacterial loads, were the beta2-microglobulin(-/-), followed by transporter associated with antigen processing deficient (TAP1(-/-)), CD8alpha(-/-), perforin(-/-), and CD1d(-/-) mice. These findings indicated that (i) CD8(+) T cells contribute to protection against MTB, and their protective activity is only partially dependent on perforin; (ii) beta2-microglobulin-dependent T cell populations distinct from CD8(+) T cells also contribute to anti-MTB immunity; and (iii) protective immune mechanisms are predominantly TAP-dependent, although TAP-independent mechanisms also contribute to protection. Because CD1d-deficient animals were fully resistant to MTB, other TAP-independent mechanisms must contribute to protection. We suggest here that both classical and nonclassical MHC class I-restricted T cells, distinct from CD1d-restricted cells, may be involved in protective immune responses against tuberculosis.

MeSH Terms
Animals CD8-Positive T-Lymphocytes/immunology Histocompatibility Antigens Class I/immunology Lung/pathology Mice Mice, Inbred C57BL Mice, Knockout Tuberculosis/immunology,prevention & control,veterinary
Chemicals
Histocompatibility Antigens Class I
Authors & Affiliations
8 authors, click to expand affiliations / ORCID
Sousa A O
Howard Hughes Medical Institute, Department of Microbiology and Immunology, Albert Einstein College of Medicine, 1300 Morris Park Avenue, Bronx, NY 10461, USA.
Mazzaccaro R J
Russell R G
Lee F K
Turner O C
Hong S
Van Kaer L
Bloom B R
References (40)
40 references, click to expand
  1. Normal development of mice deficient in beta 2M, MHC class I proteins, and CD8+ T cells.
    Science. 1990 Jun 8;248(4960):1227-30 PMID: 2112266
  2. In vitro analysis of the cellular mechanisms involved in immunity to tuberculosis.
    Rev Infect Dis. 1989 Mar-Apr;11 Suppl 2:S448-54 PMID: 2785283
  3. Memory T cell-mediated resistance to Mycobacterium tuberculosis infection in innately susceptible and resistant mice.
    Infect Immun. 1991 Jun;59(6):2012-6 PMID: 1903771
  4. MHC class I deficiency: susceptibility to natural killer (NK) cells and impaired NK activity.
    Science. 1991 Jul 12;253(5016):199-202 PMID: 1853205
  5. Effects of in vivo T lymphocyte subset depletion on mycobacterial infections in mice.
    J Leukoc Biol. 1992 Mar;51(3):225-9 PMID: 1347311
  6. Tuberculosis. Back to a frightening future.
    Nature. 1992 Aug 13;358(6387):538-9 PMID: 1501708
  7. Major histocompatibility complex class I-restricted T cells are required for resistance to Mycobacterium tuberculosis infection.
    Proc Natl Acad Sci U S A. 1992 Dec 15;89(24):12013-7 PMID: 1465432
  8. TAP1 mutant mice are deficient in antigen presentation, surface class I molecules, and CD4-8+ T cells.
    Cell. 1992 Dec 24;71(7):1205-14 PMID: 1473153
  9. Helper T cells without CD4: control of leishmaniasis in CD4-deficient mice.
    Science. 1993 Sep 10;261(5127):1448-51 PMID: 8367726
  10. An essential role for interferon gamma in resistance to Mycobacterium tuberculosis infection.
    J Exp Med. 1993 Dec 1;178(6):2249-54 PMID: 7504064
  11. Identification of a Tap-dependent leader peptide recognized by alloreactive T cells specific for a class Ib antigen.
    Cell. 1994 Nov 18;79(4):649-58 PMID: 7525079
  12. The role of interleukin-12 in acquired immunity to Mycobacterium tuberculosis infection.
    Immunology. 1995 Mar;84(3):423-32 PMID: 7751026
  13. Tumor necrosis factor-alpha is required in the protective immune response against Mycobacterium tuberculosis in mice.
    Immunity. 1995 Jun;2(6):561-72 PMID: 7540941
  14. TAP-independent, beta 2-microglobulin-dependent surface expression of functional mouse CD1.1.
    J Exp Med. 1995 Dec 1;182(6):1913-9 PMID: 7500037
  15. Identification of an H2-M3-restricted Listeria epitope: implications for antigen presentation by M3.
    Immunity. 1996 Jul;5(1):63-72 PMID: 8758895
  16. Perforin, a cytotoxic molecule which mediates cell necrosis, is not required for the early control of mycobacterial infection in mice.
    Infect Immun. 1997 Jan;65(1):127-32 PMID: 8975902
  17. Increased clearance of IgG in mice that lack beta 2-microglobulin: possible protective role of FcRn.
    Immunology. 1996 Dec;89(4):573-8 PMID: 9014824
  18. The course of Mycobacterium tuberculosis infection in the lungs of mice lacking expression of either perforin- or granzyme-mediated cytolytic mechanisms.
    Infect Immun. 1997 Apr;65(4):1317-20 PMID: 9119468
  19. CD1d1 mutant mice are deficient in natural T cells that promptly produce IL-4.
    Immunity. 1997 Apr;6(4):469-77 PMID: 9133426
  20. Differential effects of cytolytic T cell subsets on intracellular infection.
    Science. 1997 Jun 13;276(5319):1684-7 PMID: 9180075
  21. ATP-induced killing of mycobacteria by human macrophages is mediated by purinergic P2Z(P2X7) receptors.
    Immunity. 1997 Sep;7(3):433-44 PMID: 9324363
  22. Protection against Mycobacterium tuberculosis infection by CD8+ T cells requires the production of gamma interferon.
    Infect Immun. 1998 Feb;66(2):830-4 PMID: 9453650
  23. Adaptive response of iron absorption to anemia, increased erythropoiesis, iron deficiency, and iron loading in beta2-microglobulin knockout mice.
    Blood. 1998 Apr 15;91(8):3059-65 PMID: 9531620
  24. Characterization of human CD8+ T cells reactive with Mycobacterium tuberculosis-infected antigen-presenting cells.
    J Exp Med. 1998 May 18;187(10):1633-40 PMID: 9584141
  25. Listeria monocytogenes-infected hepatocytes are targets of major histocompatibility complex class Ib-restricted antilisterial cytotoxic T lymphocytes.
    Infect Immun. 1998 Jun;66(6):2814-7 PMID: 9596753
  26. Transporters associated with antigen processing (TAP)-independent presentation of soluble insulin to alpha/beta T cells by the class Ib gene product, Qa-1(b).
    J Exp Med. 1998 Sep 7;188(5):961-71 PMID: 9730897
  27. An antimicrobial activity of cytolytic T cells mediated by granulysin.
    Science. 1998 Oct 2;282(5386):121-5 PMID: 9756476
  28. Activation of human CD8+ alpha beta TCR+ cells by Mycobacterium tuberculosis via an alternate class I MHC antigen-processing pathway.
    J Immunol. 1999 Jan 1;162(1):372-9 PMID: 9886409
  29. Mice deficient in CD4 T cells have only transiently diminished levels of IFN-gamma, yet succumb to tuberculosis.
    J Immunol. 1999 May 1;162(9):5407-16 PMID: 10228018
  30. An invariant T cell receptor alpha chain defines a novel TAP-independent major histocompatibility complex class Ib-restricted alpha/beta T cell subpopulation in mammals.
    J Exp Med. 1999 Jun 21;189(12):1907-21 PMID: 10377186
  31. Susceptibility of mice deficient in CD1D or TAP1 to infection with Mycobacterium tuberculosis.
    J Exp Med. 1999 Jun 21;189(12):1973-80 PMID: 10377193
  32. Iron acquisition and metabolism by mycobacteria.
    J Bacteriol. 1999 Aug;181(15):4443-51 PMID: 10419938
  33. The majority of H2-M3 is retained intracellularly in a peptide-receptive state and traffics to the cell surface in the presence of N-formylated peptides.
    J Exp Med. 1999 Aug 2;190(3):423-34 PMID: 10430630
  34. Adoptive protection of the Mycobacterium tuberculosis-infected lung. Dissociation between cells that passively transfer protective immunity and those that transfer delayed-type hypersensitivity to tuberculin.
    Cell Immunol. 1984 Mar;84(1):113-20 PMID: 6421492
  35. The kinetics of emergence and loss of mediator T lymphocytes acquired in response to infection with Mycobacterium tuberculosis.
    J Immunol. 1987 Jan 1;138(1):293-8 PMID: 3097148
  36. Impaired resistance to Mycobacterium tuberculosis infection after selective in vivo depletion of L3T4+ and Lyt-2+ T cells.
    Infect Immun. 1987 Sep;55(9):2037-41 PMID: 3114143
  37. Mycobacteria-reactive Lyt-2+ T cell lines.
    Eur J Immunol. 1988 Jan;18(1):59-66 PMID: 2450033
  38. The secreted antigens of Mycobacterium tuberculosis and their relationship to those recognized by the available antibodies.
    J Gen Microbiol. 1988 Feb;134(2):531-8 PMID: 3139828
  39. Microbial glycolipids: possible virulence factors that scavenge oxygen radicals.
    Proc Natl Acad Sci U S A. 1989 Apr;86(7):2453-7 PMID: 2538841
  40. Lipoarabinomannan, a possible virulence factor involved in persistence of Mycobacterium tuberculosis within macrophages.
    Infect Immun. 1991 May;59(5):1755-61 PMID: 1850379
Article Info
Journal
Proceedings of the National Academy of Sciences of the United States of America
Abbr.
Proc Natl Acad Sci U S A
ISSN
0027-8424
DOI
10.1073/pnas.97.8.4204
Published
2000-04-11
Pages
4204-8
Language
English
Region
United States
NLM ID
7505876
PMCID
PMC18197
Subset
IM
Grants
NIAID NIH HHS · R01 AI007118 · United States
NIAID NIH HHS · AI 07118 · United States
NIAID NIH HHS · AI 23545 · United States
External Links
PubMed source DOI: 10.1073/pnas.97.8.4204 PMC Full Text View journal details
Analysis Services
Analysis Services

Contact

No. 2 Wenbo Road, Zhangqiu District, Jinan, Shandong

Qilu Normal University · Genelibs Bioinformatics Lab

750 Shunhua Rd, Jinan

2F, Bldg F, University Science Park

Tel: 0531-88819269

WeChat Official Account

Follow our WeChat subscription account for real-time updates and the latest in medical and biological research.


Business Email

E-mail: product@genelibs.com

Copyright © 2026.Genelibs Jinan Honghui Biotechnology Co., Ltd. 鲁ICP备20007159号-2