CD5L is upregulated upon infection with Mycobacterium tuberculosis with no effect on disease progression

CD4-Positive T-Lymphocytes Mice, Knockout Scavenger Receptors, Class A Mycobacterium tuberculosis Up-Regulation Mice, Inbred C57BL Mice Disease Models, Animal Interferon-gamma Disease Progression Animals Tuberculosis Female Lung Tuberculosis, Pulmonary Biomarkers
DOI: 10.1111/imm.13825 Publication Date: 2024-06-24T01:28:23Z
ABSTRACT
Abstract Tuberculosis (TB) alone caused over a billion deaths in the last 200 years, making it one of deadliest diseases to humankind. Understanding immune mechanisms underlying protection or pathology TB is key uncover much needed innovative approaches tackle TB. The scavenger receptor cysteine‐rich molecule CD5 antigen‐like (CD5L) has been associated with TB, but whether and how CD5L shapes response during course disease remains poorly understood. Here, we show an upregulation circulation at site infection C57BL/6 Mycobacterium tuberculosis ‐infected mice. To investigate role studied progression M. aerosol recently described genetically engineered mouse model lacking CD5L. Despite increase wild‐type mice, absence did not impact bacterial burden, histopathology survival infected Absence modest numbers CD4+ T cells expression IFN‐γ lungs no major effect overall cell dynamics. Collectively, this study confirms as potential diagnostic biomarker showing discernible on outcome infection.
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