Cutting edge:: CD1d deficiency impairs murine host defense against the spirochete, Borrelia burgdorferi

被引:144
作者
Kumar, H
Belperron, A
Barthold, SW
Bockenstedt, LK
机构
[1] Yale Univ, Sch Med, Rheumatol Sect, Dept Internal Med, New Haven, CT 06520 USA
[2] Univ Calif Davis, Sch Med, Ctr Comparat Med, Davis, CA 95616 USA
[3] Univ Calif Davis, Sch Vet Med, Ctr Comparat Med, Davis, CA 95616 USA
关键词
D O I
10.4049/jimmunol.165.9.4797
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
CD1 molecules can present microbial lipid Ag to T cells, suggesting that they participate in host defense against pathogens. hi this study, we examined the role of CD1d in resistance to infection with the Lyme disease spirochete, Borrelia burgdorferi (Bb), an organism with proinflammatory lipid Ag, Ph infection of CD1d-deficient (CD1d(-/-)) mouse strains normally resistant to this pathogen resulted in arthritis. Pathology correlated with an increased prevalence of spirochete DNA in tissues and enhanced production of Bb-specific IgG, including IgG to I-ig rapidly down-modulated on spirochetes in vivo. CD1d(-/-) Inice exhibited high-titer Bb-specific IgG2a, an isotype commonly induced in disease-susceptible mice but not in the disease-resistant control mice in this study. These results show that CD1d deficiency impairs host resistance to a spirochete pathogen, and are the first example of a mutation that imparts Ph-resistant mice with the Ab and disease profile of a susceptible mouse strain.
引用
收藏
页码:4797 / 4801
页数:5
相关论文
共 41 条
[1]  
Amano M, 1998, J IMMUNOL, V161, P1710
[2]   SPLENIC DEPENDENCE OF THE ANTIBODY-RESPONSE TO THYMUS-INDEPENDENT (TI-2) ANTIGENS [J].
AMLOT, PL ;
GRENNAN, D ;
HUMPHREY, JH .
EUROPEAN JOURNAL OF IMMUNOLOGY, 1985, 15 (05) :508-512
[3]   Murine natural killer cells contribute to the granulomatous reaction caused by mycobacterial cell walls [J].
Apostolou, I ;
Takahama, Y ;
Belmant, C ;
Kawano, T ;
Huerre, M ;
Marchal, G ;
Cui, J ;
Taniguchi, M ;
Nakauchi, H ;
Fournié, JJ ;
Kourilsky, P ;
Gachelin, G .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1999, 96 (09) :5141-5146
[4]   Protective and arthritis-resolving activity in sera of mice infected with Borrelia burgdorferi [J].
Barthold, SW ;
Feng, SL ;
Bockenstedt, LK ;
Fikrig, E ;
Feen, K .
CLINICAL INFECTIOUS DISEASES, 1997, 25 :S9-S17
[5]   LYME BORRELIOSIS IN GENETICALLY RESISTANT AND SUSCEPTIBLE MICE WITH SEVERE COMBINED IMMUNODEFICIENCY [J].
BARTHOLD, SW ;
SIDMAN, CL ;
SMITH, AL .
AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE, 1992, 47 (05) :605-613
[6]   LYME BORRELIOSIS IN SELECTED STRAINS AND AGES OF LABORATORY MICE [J].
BARTHOLD, SW ;
BECK, DS ;
HANSEN, GM ;
TERWILLIGER, GA ;
MOODY, KD .
JOURNAL OF INFECTIOUS DISEASES, 1990, 162 (01) :133-138
[7]  
BARTHOLD SW, 1993, AM J PATHOL, V143, P959
[8]   CIRCUMVENTION OF OUTER SURFACE PROTEIN-A IMMUNITY BY HOST-ADAPTED BORRELIA-BURGDORFERI [J].
BARTHOLD, SW ;
FIKRIG, E ;
BOCKENSTEDT, LK ;
PERSING, DH .
INFECTION AND IMMUNITY, 1995, 63 (06) :2255-2261
[9]  
BOCKENSTEDT LK, 1993, J IMMUNOL, V151, P900
[10]   Analysis of the lipidated recombinant outer surface protein A from Borrelia burgdorferi by mass spectrometry [J].
Bouchon, B ;
Klein, M ;
Bischoff, R ;
VanDorsselaer, A ;
Roitsch, C .
ANALYTICAL BIOCHEMISTRY, 1997, 246 (01) :52-61