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Monard, S. C.

Publications and source records attributed to Monard, S. C..

3 recordsLinked to original sources

Human cornea harbors tissue-resident memory T cells shaped by systemic immune activation, age and biological sex

The cornea is classically regarded as an immune-privileged tissue. However, recent studies have identified T cells in the healthy human cornea that are absent in specific pathogen-free (SPF) mice. The identity of these T cells, the systemic cues that drive their establishment, and the molecular mechanisms governing their corneal homing remain unknown. Here, we combine multimodal human data with tractable murine models to characterize the cellular basis of corneal immune surveillance. Immunofluorescence staining and confocal imaging of clinically non-inflamed human donor tissues revealed CD3 T cells within the corneal epithelium. Flow cytometry revealed that these cells were predominantly CD8, with a tissue-resident memory T (TRM) cell phenotype. In vivo confocal microscopy demonstrated that corneal T cell abundance increased with age, particularly in males, suggesting that accumulation is shaped by cumulative systemic immune experience. Whereas young SPF mice were devoid of corneal T cells, infection with pathogens that do not typically target the cornea induced long-lived TRM-like CD8 T cells in the cornea. We identified CXCR6 as required for efficient T cell recruitment to the cornea of viral-infected mice. Together, our human and murine data support a model in which systemic immune history, age and biological sex influence local immune surveillance at the human ocular surface.

immunology↗

Immune responses to infection modulate peripheral sympathetic neuron functions

The central nervous system interprets inflammatory signals in the body and directs the modulation of inflammatory responses by reflexively engaging peripheral sympathetic neurons1,2. This includes sympathetic neurons that innervate the spleen, which can regulate immune functions3-5 and modulate inflammation6-8. Yet, it is unclear if neuroimmune interactions involve specialised immunoregulatory sympathetic neurons, and if the immune system can reciprocally regulate peripheral sympathetic neurons to control these responses. Using retrograde tracing and single-cell transcriptomics, we find that spleen-innervating neurons are heterogeneous but do not exhibit a distinct transcriptional program indicative of specialisation for immune communication. However, we report that immune responses induced by pathogens can regulate postganglionic sympathetic neuron functions. Cytokines produced by immune cells downregulate expression of the neurotrophin nerve growth factor in spleen mesenchymal cells, leading to organ-specific sympathetic nerve retraction from the spleen. Concurrently, splenic type I interferon signalling induces inflammatory gene expression in neurons and suppresses neuron excitability. Chemogenetic activation of sympathetic neurons demonstrates an impaired anti-inflammatory capacity in the spleen during infection. These results reveal regulation of sympathetic neuronal functions by the immune system, which could support optimal generation of immune responses against pathogens.

immunology↗

The inflammasome components NLRP3 and ASC act in concert with IRGM to rearrange the Golgi during viral infections

Hepatitis C virus (HCV) infection triggers Golgi fragmentation through the Golgi-resident protein immunity-related GTPase M (IRGM). Here, we report the role of NLRP3 and ASC, two inflammasome components, in the initial events leading to this fragmentation. We show that ASC resides at the Golgi with IRGM at homeostasis. Upon infection, ASC dissociates from both IRGM and Golgi and associates with HCV-induced NLRP3. NLRP3 silencing inhibits Golgi fragmentation. ASC silencing disrupts the Golgi structure in both control and infected cells and reduces the localization of IRGM at the Golgi. Silencing IRGM cannot totally restore the Golgi structure. These data highlight a role for ASC, upstream of the formation of the inflammasome, in regulating IRGM through its control on the Golgi. A similar mechanism occurs in response to Nigericin or infection with Zika virus (ZIKV). We propose a model for a newly ascribed function of the inflammasome components in Golgi structural remodeling.

microbiology↗