Enterobacterial infection modulates major histocompatibility complex class I expression on mononuclear cells

Kirveskari, Juha; He, Qing; Leirisalo‐Repo, Marjatta; Mäki-Ikola, O; Wuorela, Maarit; Putto-Laurila, Anne; Granfors, Kaisa

doi:10.1046/j.1365-2567.1999.00803.x

Cited by 25 publications

(15 citation statements)

References 26 publications

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“…For example, a known mechanism of evasion of the host's immune system through suppression of CD8 ϩ responses is the down-regulation of expression of HLA class I molecules during viral infections and with tumors (41)(42)(43)(44). Of note, down-regulation of the expression of HLA class I molecules by enterobacterial infection, including Salmonella, Yersinia, and Klebsiella infection, has also been reported (45). In this regard, it is important to note that exposure of human primary macrophages to effector cells resulted in enhanced expression of HLA-E on their cell surface (Fig.…”

Section: Discussionmentioning

confidence: 99%

Identification of a Human HLA-E-Restricted CD8+ T Cell Subset in Volunteers Immunized withSalmonella entericaSerovar Typhi Strain Ty21a Typhoid Vaccine

Salerno-Gonçalves

Fernández-Viña

Lewinsohn³

et al. 2004

The Journal of Immunology

144

180

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Our previous studies in volunteers immunized with Salmonella enterica serovar Typhi (S. Typhi) have suggested an important role for CD8+ T cells in host defense. In this study we describe a novel subset of nonclassical human HLA-E-restricted S. Typhi-specific CD8+ T cells derived from PBMC of Ty21a typhoid vaccinees. CD3+CD8+CD4−CD56− T cells effectively killed S. Typhi-infected targets regardless of whether they share classical HLA class I molecules with them, by a FAS-independent, granule-dependent mechanism, as evidenced by induction of granzyme B release and the blocking effects of concanamycin and strontium ions. The expression of HLA-E Ags, but not CD1-a, -b, or -c, on the membrane of S. Typhi-infected targets rendered them susceptible to lysis. Moreover, anti-HLA-E Abs partially blocked these responses. We also demonstrated that presentation of S. Typhi Ags via HLA-E could stimulate IFN-γ production. Increases in the net frequency of IFN-γ spot-forming cells were observed in the presence of targets coated with peptides that contain S. Typhi GroEL HLA-E binding motifs. These results demonstrate that HLA-E binds nonamer peptides derived from bacterial proteins and trigger CD8+-mediated lysis and IFN-γ production when exposed to infected targets, raising the possibility that this novel effector mechanism might contribute to host defense against intracellular bacterial infections.

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Section: Discussionmentioning

confidence: 99%

Identification of a Human HLA-E-Restricted CD8+ T Cell Subset in Volunteers Immunized withSalmonella entericaSerovar Typhi Strain Ty21a Typhoid Vaccine

Salerno-Gonçalves

Fernández-Viña

Lewinsohn³

et al. 2004

The Journal of Immunology

144

180

View full text Add to dashboard Cite

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“…Based on the experimental and clinical data available, the apparently contradictory effects on the immune system may be explained by a bimodal action of DPP IV in immune function; immune reactions that have been initiated by other mechanisms are supported by DPP IV enzymatic activity, while other immune reactions are rather reduced, thus focusing the immunosurveillance on processes that are already under way (21). A direct participation of bacterial components in the onset of arthritis has been reported, but the mechanisms involved are unclear (18,25,26,36,43,45). It appears that exposure to a single isolated bacterial peptide is insufficient to trigger an autoimmune disease.…”

Section: Discussionmentioning

confidence: 99%

Streptokinase Promotes Development of Dipeptidyl Peptidase IV (CD26) Autoantibodies after Fibrinolytic Therapy in Myocardial Infarction Patients

Cuchacovich

Gatica

Vial

et al. 2002

Clin Vaccine Immunol

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Dipeptidyl peptidase IV (DPP IV) (CD26) plays a critical role in the modulation and expression of autoimmune and inflammatory diseases. We recently reported that sera from patients with rheumatoid arthritis and systemic lupus erythematosus contained low levels of DPP IV and high titers of anti-DPP IV autoantibodies of the immunoglobulin A (IgA) and IgG classes and found a correlation between the low circulating levels of DPP IV and the high titers of anti-DPP IV autoantibodies of the IgA class. Since streptokinase (SK) is a potent immunogen and binds to DPP IV, we speculated that patients with autoimmune diseases showed higher DPP IV autoantibody levels than healthy controls as a consequence of an abnormal immune stimulation triggered by SK released during streptococcal infections. We assessed this hypothesis in a group of patients suffering from acute myocardial infarction, without a chronic autoimmune disease, who received SK as part of therapeutic thrombolysis. Concomitant with the appearance of anti-SK antibodies, these patients developed anti-DPP IV autoantibodies. These autoantibodies bind to DPP IV in the region which is also recognized by SK, suggesting that an SK-induced immune response is responsible for the appearance of DPP IV autoantibodies. Furthermore, we determined a correlation between high titers of DPP IV autoantibodies and an augmented clearance of the enzyme from the circulation. Serum levels of the inflammatory cytokines tumor necrosis factor alpha (TNF-␣) and interleukin 6 (IL-6) increased significantly after 30 days of SK administration, while the levels of soluble IL-2 receptor remained unchanged during the same period, suggesting a correlation between the lower levels of circulating DPP IV and higher levels of TNF-␣ and IL-6 in serum in these patients.

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“…This cytotoxicity is not exerted against normal autologous nucleated cells, because surface MHC class I antigens recognize the inhibitory receptors of NK cells. On the other hand, NK cell cytotoxicity against mononuclear phagocytes infected with viruses or intracellular bacteria may reflect the fact that the pathogens lowered or modified MHC class I expression on their host cells (5,9,25). Therefore, a modification of MHC class I receptor at the surface of Brucella-infected macrophages could account for the cytolytic activation of NK cells.…”

Section: Discussionmentioning

confidence: 99%

Impairment of IntramacrophagicBrucella suisMultiplication by Human Natural Killer Cells through a Contact-Dependent Mechanism

et al. 2004

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Brucellosis is a worldwide zoonosis that affects domestic animals and humans. The pathogenesis exhibited by this disease differs remarkably between humans and animals (35, 43). In domestic animals, brucellosis is mainly an abortive disease that results from a long-lasting often-unapparent infection. On the other hand, human brucellosis, also named Malta fever, is a complex disease that begins with a systemic infection that can be followed either by localized infection or chronic disease (15,29,43). Murine models are commonly used to study Brucella infection. Many strains of mice are sensitive to Brucella spp. but develop a disease quite different from that observed in domestic animals or in humans. Infection with Brucella does not modify pregnancy in mice, and acute infection results in a long-lasting presence of bacteria in the spleen and liver, predominantly. In humans, chronic infection is characterized by a specific bacterial localization within the body (spleen, liver, heart, bones, and brain) and a deleterious effect of the bacteria on these organs (43). The difference in pathogeny results most likely from differences in the immune responses in humans, domestic animals, and animal models (14). Some important differences between the immune responses of mice and humans have been reported. Brucella suis inhibits macrophage tumor necrosis factor alpha (TNF-␣) production in humans but not in mice (7,8) and this property is due to the outer membrane protein Omp25 (23). Furthermore, humans possess a specific type of circulating lymphocytes, called T␥9␦2, which is absent in mice. These lymphocytes proliferate importantly in human blood after Brucella infection (2) and impair intramacrophagic multiplication (36, 37).The mouse immune response has been widely studied (1, 19) although the reasons for the persistence of Brucella are not understood (22). The immune response in mammals can be divided into innate and adaptive immunity. Although the adaptive immunity is the most efficient response to eliminate infectious agents, it is widely accepted that innate response determines the behavior of specific response particularly in defining Th1 versus Th2 polarized response. Thus, the innate response is very important for the evolution of the infection. The importance of the Th1 cytokine gamma interferon (IFN-␥) in controlling infection in mice has been emphasized (1, 33). Among the cells involved in IFN-␥ production, NK cells play a particular role; they are the most important IFN-␥ producers in the beginning of infection. However, it has been clearly demonstrated that NK cells do not play a major role in the early control of Brucella abortus infection in mice (18). On the other hand, it was formally established that in the acute phase of the illness, the activity of the NK cells is impaired in humans developing brucellosis (40). Moreover, human NK cells were recently shown to mediate the intracellular killing of Mycobacterium tuberculosis (4). Therefore, in order to better understand the role of NK cells in bacterial deve...

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Enterobacterial infection modulates major histocompatibility complex class I expression on mononuclear cells

Cited by 25 publications

References 26 publications

Identification of a Human HLA-E-Restricted CD8+ T Cell Subset in Volunteers Immunized withSalmonella entericaSerovar Typhi Strain Ty21a Typhoid Vaccine

Identification of a Human HLA-E-Restricted CD8+ T Cell Subset in Volunteers Immunized withSalmonella entericaSerovar Typhi Strain Ty21a Typhoid Vaccine

Streptokinase Promotes Development of Dipeptidyl Peptidase IV (CD26) Autoantibodies after Fibrinolytic Therapy in Myocardial Infarction Patients

Impairment of IntramacrophagicBrucella suisMultiplication by Human Natural Killer Cells through a Contact-Dependent Mechanism

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