Autoantibody Reactivity in Hidradenitis Suppurativa: Characterizing Keratinocyte and Apocrine Gland Targets Across Disease Progression and Anti-TNF-α Treatment

Author

• Talla Hamouche, CUNY Bernard M Baruch CollegeFollow

Date of Award

Spring 4-27-2026

Document Type

Thesis

Degree Name

B.A.

Honors Designation

yes

Program of Study

Biology

Language

English

First Advisor

Catherine Pei-ju Lu

Second Advisor

Pablo M. Peixoto

Abstract

Hidradenitis suppurativa (HS) is a chronic, relapsing inflammatory skin disease associated with impaired quality of life, representing one of the highest burdens among dermatological conditions. This debilitating disorder primarily affects apocrine-gland-bearing and flexural skin areas, most commonly the axillae, breast, buttocks, and groin. As lesions recur and new sites emerge, surgical excision does not guarantee prevention of disease reestablishment. Despite its substantial burden, HS remains among the least understood and most treatment-resistant inflammatory diseases. The mechanisms underlying this chronicity and the frequent failure of conventional anti-inflammatory therapies remain unresolved. An underappreciated autoimmune dimension may contribute to HS pathogenesis: the clonal expansion of plasma cells within tertiary lymphoid structures in lesional skin, generating antibodies directed against the patient’s own epithelial cells. This thesis presents a longitudinal investigation of these autoantibodies across two episodes of disease recurrence in patients before and after treatment with Humira, tracking the evolution of the autoimmune humoral response under anti-TNF-α therapy. Patient- derived antibodies isolated from clonally expanded plasma cells at each time point were used to map autoantibody reactivity across multiple tissue compartments. Complementary single-cell RNA and V(D)J sequencing data from the same patients reveal corresponding shifts in immune cell composition between disease recurrences, providing a transcriptomic framework for interpreting the antibody-level findings. These data indicate that TNF-α blockade does notuniformly suppress the autoimmune humoral response in HS, that apocrine glands represent a previously uncharacterized site of autoantigen expression, and that the persistence of tissue- targeted autoantibodies across treatment cycles may be a key driver of the chronic, recurrent nature of this disease.

Recommended Citation

Hamouche, Talla, "Autoantibody Reactivity in Hidradenitis Suppurativa: Characterizing Keratinocyte and Apocrine Gland Targets Across Disease Progression and Anti-TNF-α Treatment" (2026). CUNY Academic Works.
https://academicworks.cuny.edu/bb_etds/224