Deciphering the role of calcium homeostasis in T cells functions during mycobacterial infection
Autor: | Krishnamurthy Natarajan, Vandana Anang, Aarti Singh, Ankush Kumar Rana, Shakuntala Surender Kumar Saraswati, Aayushi Singh, Priyanka Kumari, Chaitenya Verma |
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Rok vydání: | 2020 |
Předmět: |
0301 basic medicine
T-Lymphocytes medicine.medical_treatment T cell Immunology chemistry.chemical_element Apoptosis Biology Calcium Lymphocyte Activation Mycobacterium Mice 03 medical and health sciences 0302 clinical medicine Immune system Autophagy medicine Animals Homeostasis Tuberculosis Calcium metabolism Mice Inbred BALB C Mycobacterium Infections Voltage-dependent calcium channel Effector Macrophages Mycobacterium tuberculosis Cell biology 030104 developmental biology Cytokine medicine.anatomical_structure chemistry Cytokines Interleukin-2 Female Calcium Channels 030215 immunology |
Zdroj: | Cellular Immunology. 357:104198 |
ISSN: | 0008-8749 |
DOI: | 10.1016/j.cellimm.2020.104198 |
Popis: | Calcium plays an important role in regulating cell physiology and immune responses to various pathogens. Our recent work has highlighted the crucial role for calcium homeostasis in dendritic cells and macrophages during various infections. Here we investigated the effect of calcium homeostasis in regulating T cell activation and function during mycobacterial infection. Results show that calcium homeostasis had varied effects in regulating T cell activation and function during mycobacterial infection. This included regulation of the expression of co-stimulatory molecules, cytokine profiles and effector function. A net negative role for Voltage Gated Calcium Channel (VGCC) was observed. Inhibiting VGCC in mycobacteria primed T cells induced increased production of pro-inflammatory cytokines and an increased effector phenotype. Infected macrophages when incubated with VGCC inhibited T cells, induced increased expression of co-stimulatory molecule expression on macrophages, increased the production of pro-inflammatory cytokines and increased autophagy and apoptosis. This collectively led to reduced survival of mycobacteria inside macrophages. The data point towards a fine regulation of protective responses by routes of calcium influx and release that mediate pathogen survival or clearance. |
Databáze: | OpenAIRE |
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