Hidradenitis suppurativa (HS) is a chronic inflammatory disease of the pilosebaceous unit which, by its recurrent course, pain, unpleasant odour and aesthetic deficiencies, dramatically reduces patient's quality of life. It most often reaches its peak incidence in the early twenties or thirties. The etiopathogenesis of disease has not yet been fully elucidated. Still, it is known that it is multifactorial disease in which inadequate tissue immune response, in combination with risk factors including overweight, smoking, mechanical irritation and genetic factors, plays a key role. Follicle occlusion results in dilatation, rupture and release of follicular content into the dermis. Cellular debris, bacteria and sebum stimulate inflammatory cells, mostly macrophages and neutrophils, to enhanced synthesis and secretion of matrix metalloproteinases, antimicrobial peptides and numerous cytokines, among which, by their role, TNF-α and IL-17 stand out the most. Clinical picture of HS is characterized by painful subcutaneous nodules that progress to deep abscesses, drainage sinuses, and hypertrophic scars and contractures in the intertriginous areas. Diagnosis is made clinically, based on the case history, characteristic skin lesions and their topography. According to European guidelines, the treatment of HS can be medicamentous, surgical, laser and a combination of these treatment modalities. The form of used therapy depends on the severity of the clinical picture, the degree of skin involvement and the patient's comorbidities. Aim of this thesis is to present current evidence in the pathogenesis of HS through the cascade of autoinflammatory reactions, activated by signaling pathways, which manifests in the form of chronic inflammatory skin disease.