CCR2 recruits monocytes to the lung, while CX3CR1 modulates positioning of monocyte-derived CD11cposcells in the lymph node during pulmonary tuberculosis DOI Open Access
Alexander Mohapatra,

Zachary Howard,

J. Ernst

et al.

bioRxiv (Cold Spring Harbor Laboratory), Journal Year: 2025, Volume and Issue: unknown

Published: Feb. 8, 2025

ABSTRACT Infection by Mycobacterium tuberculosis (Mtb) continues to cause more than 1 million deaths annually, due pathogen persistence in lung macrophages and dendritic cells derived from blood monocytes. While accumulation of monocyte-derived the Mtb-infected partially depends on chemokine receptor CCR2, other chemoattractant receptors regulating trafficking remain undefined. We used mice expressing knock-in/knockout reporter alleles Ccr2 Cx3cr1 interrogate their expression function populations lungs draining mediastinal lymph nodes during Mtb infection. CCR2 CX3CR1 varied across subsets stratified cell surface Ly6C both organs. found that predicted dependence for node accumulation. CCR2-deficient were also observed have worsened burden. deficiency, alone or combination with did not affect frequencies control, its absence was associated altered positioning nodes. combined loss control node, suggesting a rationale persistent among pulmonary tuberculosis. IMPORTANCE is respiratory responsible deadliest infectious disease worldwide. Susceptible humans exhibit ineffective immune responses, which infected phagocytes are able eliminate pathogen. Since recruited serve as reservoirs infection, understanding how these accumulate why they unable can inform development therapies synergize antimicrobials achieve faster durable elimination. Monocyte-derived express CX3CR1, but role latter infection remains poorly defined. The significance our study elucidating roles node. These data shed light host response infections.

Language: Английский

CCR2 recruits monocytes to the lung, while CX3CR1 modulates positioning of monocyte-derived CD11cposcells in the lymph node during pulmonary tuberculosis DOI Open Access
Alexander Mohapatra,

Zachary Howard,

J. Ernst

et al.

bioRxiv (Cold Spring Harbor Laboratory), Journal Year: 2025, Volume and Issue: unknown

Published: Feb. 8, 2025

ABSTRACT Infection by Mycobacterium tuberculosis (Mtb) continues to cause more than 1 million deaths annually, due pathogen persistence in lung macrophages and dendritic cells derived from blood monocytes. While accumulation of monocyte-derived the Mtb-infected partially depends on chemokine receptor CCR2, other chemoattractant receptors regulating trafficking remain undefined. We used mice expressing knock-in/knockout reporter alleles Ccr2 Cx3cr1 interrogate their expression function populations lungs draining mediastinal lymph nodes during Mtb infection. CCR2 CX3CR1 varied across subsets stratified cell surface Ly6C both organs. found that predicted dependence for node accumulation. CCR2-deficient were also observed have worsened burden. deficiency, alone or combination with did not affect frequencies control, its absence was associated altered positioning nodes. combined loss control node, suggesting a rationale persistent among pulmonary tuberculosis. IMPORTANCE is respiratory responsible deadliest infectious disease worldwide. Susceptible humans exhibit ineffective immune responses, which infected phagocytes are able eliminate pathogen. Since recruited serve as reservoirs infection, understanding how these accumulate why they unable can inform development therapies synergize antimicrobials achieve faster durable elimination. Monocyte-derived express CX3CR1, but role latter infection remains poorly defined. The significance our study elucidating roles node. These data shed light host response infections.

Language: Английский

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