Pubblicazioni

Autori:

Costa, S; Marini, O; Bevilacqua, D; Defranco, Al; Hou, B; Lonardi, S; Vermi, W; Rodegher, P; Panato, A; Tagliaro, F; Lowell, Ca; Cassatella, Marco Antonio; Girolomoni, Giampiero; Scapini, P.

Titolo:

Role of MyD88 signaling in the imiquimod-induced mouse model of psoriasis: focus on innate myeloid cells.

Anno:

2017

Tipologia prodotto:

Articolo in Rivista

Tipologia ANVUR:

Articolo su rivista

Lingua:

Inglese

Formato:

A Stampa

Referee:

No

Nome rivista:

Journal of Leukocyte Biology

ISSN Rivista:

0741-5400

N° Volume:

102

Numero o Fascicolo:

3

Intervallo pagine:

791-803

Parole chiave:

monocytes/macrophages; neutrophils; skin inflammation

Breve descrizione dei contenuti:

Psoriasis is a chronic skin disease associated with deregulated activation of immune cells and keratinocytes. In this study, we used the imiquimod (IMQ)-induced mouse model of psoriasis to dissect better the contribution of hematopoietic and skin-resident stromal cells to psoriasis development. The comparison of disease development in mice carrying the hematopoietic cell-specific deletion of MyD88 (Myd88fl/flVav-cre+ mice) with mice carrying the total MyD88 deficiency (Myd88-/- mice), we show that the progression of skin and systemic inflammation, as well as of epidermal thickening, was completely dependent on MyD88 expression in hematopoietic cells. However, both Myd88-/- mouse strains developed some degree of epidermal thickening during the initial stages of IMQ-induced psoriasis, even in the absence of hematopoietic cell activation and infiltration into the skin, suggesting a contribution of MyD88-independent mechanisms in skin-resident stromal cells. With the use of conditional knockout mouse strains lacking MyD88 in distinct lineages of myeloid cells (Myd88fl/flLysM-cre+ and Myd88fl/flMRP8-cre+ mice), we report that MyD88 signaling in monocytes and Mϕ, but not in neutrophils, plays an important role in disease propagation and exacerbation by modulating their ability to sustain γδ T cell effector functions via IL-1β and IL-23 production. Overall, these findings add new insights into the specific contribution of skin-resident stromal vs. hematopoietic cells to disease initiation and progression in the IMQ-induced mouse model of psoriasis and uncover a potential novel pathogenic role for monocytes/Mϕ to psoriasis development.

Id prodotto:

98789

Handle IRIS:

11562/968131

ultima modifica:

15 novembre 2022

Citazione bibliografica:

Costa, S; Marini, O; Bevilacqua, D; Defranco, Al; Hou, B; Lonardi, S; Vermi, W; Rodegher, P; Panato, A; Tagliaro, F; Lowell, Ca; Cassatella, Marco Antonio; Girolomoni, Giampiero; Scapini, P., Role of MyD88 signaling in the imiquimod-induced mouse model of psoriasis: focus on innate myeloid cells. «Journal of Leukocyte Biology» , vol. 102 , n. 3 , 2017 , pp. 791-803

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