There are numerous mechanisms hypothesized to be responsible in pathogenesis of<unk> . One of the prominent<unk>  pathogenesis seems to be inflammatory processes due to increased immune cells activity. Basophils, mast cells, macrophages, neutrophils and T cells are some of the most common immune cells known to be responsible in pathogenesis of<unk> . Among them, basophils and mast cells have more eminent role in<unk>  development and their activation has been related to some intracellular signal defect and/or autoimmune disorders. Some immunoglobins, such as IgE have been detected in patients suffering from<unk> . For instance , IgE anti-IL-24 is one of these IgE autoantigens that have been found in all patients with chronic spontaneous<unk> . Moreover, complement system is also responsible in pathogenesis of chronic spontaneous<unk>  and role of some complements, such as C3, C4 and C5 have been established. Based on numerous studies,<unk>  patients may have some genetical changes. Upregulation of 506 genes and downregulation of 51 genes have been reported in the affected skin with chronic spontaneous<unk> . Most of the upregulated genes were involve in adhesion (such as SELE (1q24), cell activation (such as CD69), and chemotaxis (such as CCL2). It is crystal clear that<unk>  is associated with autoimmune diseases such as hashimoto's thyroiditis. Other associations are mastocytisis such as<unk>  pigmentosa, atopic diseases such as atopic dermatitis, hay fever and allergic asthma and systemic lupus erythematosus and angioedema.
Urticaria pathophysiology
Tularemia pathophysiology
Rhinitis pathophysiology
Strep throat pathophysiology
Herpes simplex pathophysiology
Group A streptococcal infection pathophysiology
Hand-foot-and-mouth disease pathophysiology
Roseola pathophysiology