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[The correlation between dendritic cell-specific ICAM-3 grabbing nonintegrin expression and Mycobacterium
Jie Zhang1, Shu-liang Guo, Yong-ai Luo
1Department of Respiratory Medicine, First Affiliated Hospital, Chongqing Medical University, Chongqing, China.
Insights
Tuberculosis patients show higher expression of dendritic cell-specific ICAM-3 grabbing nonintegrin (DC-SIGN) and IL-10, leading to impaired T lymphocyte response and immune dysfunction.
Area of Science:
- Immunology
- Infectious Diseases
Context:
- Tuberculosis remains a significant global health challenge.
- Dendritic cells (DCs) play a crucial role in initiating immune responses.
- DC-SIGN is a C-type lectin receptor expressed on DCs involved in pathogen recognition.
Purpose:
- To investigate the correlation between DC-SIGN expression and Mycobacterium tuberculosis infection in humans.
- To assess DC maturation markers, cytokine profiles, and T cell proliferation in tuberculosis patients.
Summary:
- Tuberculosis patients exhibited significantly lower CD86 expression and higher DC-SIGN expression and mRNA levels on DCs compared to pneumonia patients and healthy individuals.
- DCs from tuberculosis patients secreted higher levels of IL-10 and showed reduced capacity for T lymphocyte proliferation induction.
- No significant differences were observed in CD11c, HLA-DR expression, or IL-12 levels among the groups.
Impact:
- Elevated DC-SIGN expression and IL-10 secretion by DCs may contribute to decreased DC maturity and impaired T cell-mediated immunity in tuberculosis.
- Findings suggest DC-SIGN as a potential factor in the pathogenesis of tuberculosis and immune evasion.
- This research highlights the complex interplay between DC-SIGN, cytokine production, and immune response in tuberculosis.
Objective:
To investigate the correlation between dendritic cell-specific ICAM-3 grabbing nonintegrin (DC-SIGN) expression and Mycobacterium tuberculosis in humans.
Methods:
The peripheral blood mononuclear cells were obtained respectively from 25 patients with tuberculosis, 25 patients with pneumonia and 25 healthy individuals, and were cultured in medium with GM-CSF and IL-4. Five days later, expression of CD(11c), CD(86), HLA-DR and DC-SIGN were detected by flow cytometry. The expression of DC-SIGN mRNA was detected by RT-PCR. The levels of IL-12 and IL-10 in the supernatants were measured by enzyme-linked immunosorbent assay (ELISA). Proliferation induction of T lymphocytes dendritic cells (DCs) was measured by mixed lymphocyte reaction (MLR).
Results:
The expression of CD(86) on DCs in the tuberculosis patients [(72 +/- 11)%] was significantly lower than those in the other 2 groups [(87 +/- 16)%, (92 +/- 6)%] (F = 11.97, P < 0.01). In patients with tuberculosis, the expression of DC-SIGN on DCs [(85 +/- 8)%] was significantly higher than the other 2 groups [(60 +/- 28)%, (62 +/- 13)%] (F = 8.27, P < 0.01), and so was the DC-SIGN mRNA level (F = 3.99, P < 0.05). The levels of IL-10 secreted by DCs in the tuberculosis patients [(98 +/- 31) ng/L] were significantly higher than those in the other 2 groups [(74 +/- 38) ng/L and (66 +/- 27) ng/L] (F = 4.19, P < 0.05). MLR showed lower potency of proliferation induction of T lymphocytes in the tuberculosis patients (1858 +/- 628) than the other 2 groups (3066 +/- 1389), (3383 +/- 1163) (F = 7.92, P < 0.01). Expression of CD(11c) and HLA-DR on DCs and IL-12 levels were not significantly different among the 3 groups (P > 0.05).
Conclusion:
The decreased DC maturity, elevated IL-10 secretion by DCs, decreased proliferation induction of T lymphocytes and impaired immune response may be due to overexpression of DC-SIGN in patients with tuberculosis.
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