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Immunometabolic Circuits in Infection for Advancing Host Directed Therapies
Published on: September 13, 2024
Interleukin-15 correlates with cytotoxic immune networks in cervical tuberculous lymphadenitis
Soumaya Bchiri1,2,3, Khadija Bahrini1,2, Rosane M B Teles4,5
1Laboratory of Transmission Control and Immunobiology of Infections, Institut Pasteur de Tunis, Tunis, Tunisia.
Insights
Interleukin-15 (IL-15) is identified as a key regulator of cytotoxic immune responses in cervical tuberculous lymphadenitis (CTL). This finding offers insights into the immune mechanisms underlying CTL and potential therapeutic targets.
Area of Science:
- Immunology
- Infectious Diseases
- Molecular Biology
Background:
- Cervical tuberculous lymphadenitis (CTL) is a localized form of tuberculosis (TB) where immune responses occur in lymphoid tissue.
- The cytokine networks controlling cytotoxic lymphocyte responses in human lymph node TB are not fully understood.
Purpose of the Study:
- To investigate the immune pathways and cytokine networks involved in the immunopathogenesis of CTL.
- To identify key molecular players coordinating cytotoxic immunity in human lymph node TB.
Main Methods:
- Integrated immune profiling of patients with CTL and non-tuberculous lymphadenopathy (CNTL).
- Quantification of immune-gene expression in peripheral blood and lymph node cells using qPCR.
- Systems-level analyses (principal component, correlation-network) and serum IL-15 measurement (ELISA).
- Immunohistochemistry for IL-15 and IL-15Rα tissue localization.
Main Results:
- CTL exhibits a distinct cytotoxic immune program involving granulysin, granzyme B, perforin, IFN-γ, and CCL5.
- Interleukin-15 (IL-15) emerged as a central hub in the cytotoxic module of CTL.
- Elevated IL-15 transcripts and serum concentrations were observed in CTL patients, correlating with cytotoxic genes and bacillary load.
- IL-15 and IL-15Rα were localized to macrophages within granulomatous regions in lymph nodes.
Conclusions:
- IL-15 is identified as a potential central organizer of cytotoxic immune pathways in cervical tuberculous lymphadenitis.
- IL-15-associated immune signatures provide biologically informative insights into CTL immunopathogenesis.
Introduction:
Cervical tuberculous lymphadenitis (CTL) represents a localized manifestation of Mycobacterium tuberculosis infection in which immune responses are organized within lymphoid tissue. While cytotoxic lymphocyte responses contribute to antimycobacterial immunity, the cytokine networks coordinating these responses in human lymph node tuberculosis remain incompletely defined.
Methods:
We performed integrated immune profiling of patients with CTL (n = 60) and non-tuberculous cervical lymphadenopathy (CNTL; n = 44). Immune-gene expression was quantified in peripheral blood and lymph node mononuclear cells by qPCR. Systems-level analyses including principal component and correlation-network approaches were used to define coordinated immune pathways. Serum IL-15 was measured by ELISA, and tissue localization of IL-15 and IL-15Rα was examined by immunohistochemistry.
Results:
CTL was characterized by a structured cytotoxic immune program enriched for granulysin, granzyme B, perforin, IFN-γ, and CCL5. Network analysis identified IL-15 as a highly connected hub within this cytotoxic module in CTL. IL-15 transcripts were significantly elevated in both blood and lymph node compartments (p = 0.0003; p = 0.0007, respectively) and strongly correlated with cytotoxic effector genes. Circulating IL-15 concentrations were higher in CTL than CNTL (p < 0.0001) and increased with GeneXpert-defined bacillary burden (AUC 0.73). Immunohistochemistry demonstrated IL-15 and IL-15Rα expression within CD68+ macrophages localized to granulomatous regions, consistent with macrophage-mediated IL-15 trans-presentation within sites of infection.
Conclusions:
These findings identify IL-15 as a potential central organizer of cytotoxic immune pathways in CTL and highlight IL-15-linked immune signatures as biologically informative features of CTL immunopathogenesis.
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