Type 3 immunity: a perspective for the defense of the mammary gland against infections
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OPINION
Type 3 immunity: a perspective for the defense of the mammary gland against infections Pascal Rainard1* , Patricia Cunha1, Rodrigo P. Martins1, Florence B. Gilbert1, Pierre Germon1 and Gilles Foucras2
Abstract Type 3 immunity encompasses innate and adaptive immune responses mediated by cells that produce the signature cytokines IL-17A and IL-17F. This class of effector immunity is particularly adept at controlling infections by pyogenic extracellular bacteria at epithelial barriers. Since mastitis results from infections by bacteria such as streptococci, staphylococci and coliform bacteria that cause neutrophilic inflammation, type 3 immunity can be expected to be mobilized at the mammary gland. In effect, the main defenses of this organ are provided by epithelial cells and neutrophils, which are the main terminal effectors of type 3 immunity. In addition to theoretical grounds, there is observational and experimental evidence that supports a role for type 3 immunity in the mammary gland, such as the production of IL-17A, IL-17F, and IL-22 in milk and mammary tissue during infection, although their respective sources remain to be fully identified. Moreover, mouse mastitis models have shown a positive effect of IL-17A on the course of mastitis. A lot remains to be uncovered before we can safely harness type 3 immunity to reinforce mammary gland defenses through innate immune training or vaccination. However, this is a promising way to find new means of improving mammary gland defenses against infection. Keywords: type 3 immunity, IL-17, Th17, mastitis, dairy ruminants, mammary gland A novel approach is required to improve mastitis vaccines Mastitis is the most frequent and economically important disease of dairy ruminants worldwide [1]. The main bacteria responsible for mammary gland (MG) infections (staphylococci, streptococci, and coliform bacteria) can cause acute clinical mastitis, but more often subclinical long-lasting infection and inflammation [2]. Both types of infections are characterized by the recruitment of leukocytes, mainly neutrophils, into the mammary tissue and secretions. The mechanisms behind this recruitment are incompletely defined, and although several MG defenses have been identified, their coordination and regulation at the cellular and molecular levels are insufficiently *Correspondence: [email protected] 1 ISP, INRAE, Université de Tours, UMR1282, Tours, Nouzilly, France Full list of author information is available at the end of the article
understood. Besides, despite many attempts at devising efficacious vaccines, those presently licensed do not fulfill all expectations [2, 3]. We need novel approaches that could offer new development perspectives. We propose that putting the stress on type 3 immunity, its signature cytokines and the cells that produce them or respond to them, could help fulfill this need. In this position paper, we present the reasons that make type 3 immunity a likely major mechanism of MG defense against infection, and we describe the ob
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