And the Skin Immune System

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The involvement of the immune system in HS remains controversial. Immunological investigations of some patients with HS suggested no abnormalities of the immune system [15]. In contrast, other authors showed increased peripheral suppressor T cell activity [48], suggestive of a precipitating cell-mediated immune response. This is further supported by the presence of activated, HLA-DR-positive lymphocytes [8]. Although in lower numbers and preferentially located in the direct perivascular compartment, Leu-8-positive immunoregula-tory lymphocytes were also present in lesions, suggestive of a loss of Leu-8 cellular antigen in lymphocytes during further migration into the dermal tissue [8]. These results indicate that the lymphocytic infiltrate is definitely the result of in vivo activation of lymphoid cells. Indeed, the significant fall of the T-helper/suppressor ratio over time after the initiation [8] supports the existence of a precipitating cell-mediated immune response with only a short eliciting period. Even though more recent studies have shown that dysfunctional neutrophils may also be involved in the pathogenesis of HS, no primary abnormalities of the innate or acquired immune sys

Hidradenitis Suppurativa Immune System

Fig. 13.3. Co-operative recognition of microbial-de-rived PAMPs by TLRs. Host cells use multiple TLRs for the detection of several unique features of the single microbe simultaneously. TLR4/4 and TLR5 detect LPS (a) and flagellin (b), respectively, from a flagellated Gramnegative organism (e.g., Salmonella typhi), whereas TLR5 and TLR2/6 detect flagellin (b) and diacyl-lipopeptide

(c) of another flagellated Gram-negative organism (e.g., Helicobacter pylori). Keratinocytes may also recognize Hsp and lipoglycans/lipoarabinomannans (d) from the skin pathogens P. acnes and Mycobacterium tuberculosis via TLR4/4 and TLR2/6. (Hsp Heat-shock protein, TLR Toll-like receptor)

Fig. 13.3. Co-operative recognition of microbial-de-rived PAMPs by TLRs. Host cells use multiple TLRs for the detection of several unique features of the single microbe simultaneously. TLR4/4 and TLR5 detect LPS (a) and flagellin (b), respectively, from a flagellated Gramnegative organism (e.g., Salmonella typhi), whereas TLR5 and TLR2/6 detect flagellin (b) and diacyl-lipopeptide

(c) of another flagellated Gram-negative organism (e.g., Helicobacter pylori). Keratinocytes may also recognize Hsp and lipoglycans/lipoarabinomannans (d) from the skin pathogens P. acnes and Mycobacterium tuberculosis via TLR4/4 and TLR2/6. (Hsp Heat-shock protein, TLR Toll-like receptor)

tem can be held to be causal in every case [8, 34, 42].

In addition, the significance of bacterial findings in HS is also controversial. It is generally accepted that the bacterial involvement is not a primary pathogenic event in HS, but rather it is likely that the chronic inflammation is due to secondary bacterial colonization [34]. This is further supported by the fact that routine cultures from the surface of the lesions are often negative. Still, bacteria are likely to be involved in the pathogenesis of the disease since numerous bacteria, such as S. aureus and coagulase-

negative staphylococci, are most frequently isolated from lesions [35, 41]. These findings highlight a possible polymicrobial nature and predominance of anaerobic bacteria in HS, supporting the role of bacterial infections as a possible pathogenic event in HS. Microbial colonization may, in turn, trigger several events of the skin immune response, such as secretion of antimicrobial peptides and pro-inflammatory cy-tokines/chemokines by keratinocytes through the activation of TLR/IL-1R-NF-kB signaling (Fig. 13.3). These mediators either kill the pathogens or link innate and acquired immunity by the recruitment of effector cells, such as memory T cells and dendritic cells, to the sites of infection (Fig. 13.3). Besides, keratinocyte-derived IL-8 and pro-inflammatory cytokines activate endothelial cells, allowing the transepithelial migration of neutrophils. After extravasation neutrophils follow the chemotactic gradient formed by IL-8 toward the site of infection. Infiltration of neutrophils, dendritic cells, and T cells into the epidermis may contribute not only to the elimination of the invading pathogens but, as a result of constant activation by kerati-nocyte-derived mediators, to chronic inflammation as well (Fig. 13.3).

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