222 Whole-blood immune profile in hidradenitis suppurativa

Authors

Peter Dimitrion, Henry Ford HealthFollow
Congcong Yin, Henry Ford HealthFollow
Kalpana Subedi, Henry Ford HealthFollow
Namir Khalasawi, Henry Ford HealthFollow
Yi Yao, Henry Ford HealthFollow
Angie Parks-Miller, Henry Ford HealthFollow
Jesse Veenstra, Henry Ford HealthFollow
Gautham Vellaichamy, Henry Ford HealthFollow
Henry W. Lim, Henry Ford HealthFollow
Iltefat Hamzavi, Henry Ford HealthFollow
Li Zhou, Henry Ford HealthFollow
Qing-Sheng Mi, Henry Ford HealthFollow

Recommended Citation

Dimitrion P, Yin C, Subedi K, Khalasawi N, Yao Y, Miller A, Veenstra J, Vellaichamy G, Lim H, Hamzvi I, Zhou L, and Mi Q. 222 Whole-blood immune profile in hidradenitis suppurativa. Journal of Investigative Dermatology 2021; 141(5):S39.

Document Type

Conference Proceeding

Publication Date

5-1-2021

Publication Title

Journal of Investigative Dermatology

Abstract

Hidradenitis suppurativa (HS), a chronic inflammatory skin condition with a multifactorial etiology, has a complex cutaneous immune reaction localized around the hair follicles in intertriginous skin. HS pathogenesis remains enigmatic, although some hypotheses have been proposed. Increasing evidence of the association between HS and other inflammatory conditions (e.g. inflammatory bowel disease) and cardiovascular disease suggests that patients with HS have underlying systemic inflammation. To date, few studies have sought to understand the systemic changes that occur in the immune system of HS patients. One recent study performed bulk RNA-sequencing on peripheral blood mononuclear and showed minor differences in transcriptomes of peripheral blood mononuclear cells, but bulk RNA-sequencing does not have the capacity to identify specific changes in cellular subsets. To determine whether specific systemic changes occur in HS patients we performed CyTOF using a standardized panel that identifies 37 immune cell subpopulations in whole blood. We analyzed whole blood samples from 8 HS and 7 healthy controls. Compared to healthy controls, HS patients had an increased frequency of plasmablasts and a decreased frequency of CD66b- neutrophils. Furthermore, marked differences in monocyte subclasses showed a shift from classical monocytes (CD14+ CD16-) towards intermediate (CD14+ CD16+) and non-classical subsets (CD14dim CD16+) in HS. We also identified a large population of CDR45RO+ CCR6+ CD38+ intermediate monocytes in HS, which was largely absent in healthy controls. Taken together our results support previous studies highlighting the role of neutrophils and B cells in HS pathogenesis, and identify newly discovered monocyte dynamics in peripheral blood of HS patients further supporting widespread inflammation as a feature of HS.

Volume

141

Issue

5

First Page

S39