Main mechanisms and dualism of inflammation
The pathogenesis of atopic dermatitis is based on the dominance of IgE-mediated reactions. Allergens enter the bloodstream due to intestinal barrier dysfunction, which is characteristic of early age. In response, plasma cells begin to synthesize specific IgE.
The inflammatory process occurs in two forms:
- Acute inflammation: caused by immediate-type reactions (IgE-dependent). Morphologically, this is characterized by exudation, edema, and hyperemia.
- Chronic inflammation: accompanied by the addition of a delayed-type hypersensitivity reaction. It is characterized by macrophage activation and Th1-lymphocyte proliferation.
Pathogenesis phases
The development of the process is divided into two consecutive stages:
- Sensitization phase (primary contact). The body recognizes the allergen. Naive T lymphocytes differentiate into Th2 lymphocytes, and B lymphocytes transform into plasma cells that secrete IgE.
- Manifestation phase (repeated contact). The allergen enters the skin or mucous membranes of a sensitized organism again. Specific T lymphocytes are activated in the skin tissues, triggering an immune cascade with the development of acute inflammation.
Immune-cellular profile and response switching
Depending on the stage, the prevailing type of immune response changes (the so-called Th2/Th1 switch):
- In the acute stage, the Th2 response dominates. Antigens are presented by Langerhans cells. Activated Th2 cells secrete cytokines (IL-4, IL-5, IL-13, TSLP) that stimulate the endothelium and keratinocytes. Effector cells are mast cells (releasing mediators upon binding to IgE) and eosinophils. Cytokines increase vascular permeability, causing leukocyte diapedesis into the dermis and epidermis.
- During chronic progression, there is a shift toward a Th1 response. A delayed-type hypersensitivity (DTH) reaction develops. IFN-γ and IL-12 become key cytokines, while activated macrophages predominate among effector cells.
Role of the skin barrier and sensitization pathways
Structural and functional inferiority of the skin is a crucial link in pathogenesis. The skin of patients is characterized by xerosis ( dryness) and the absence of a full-fledged hydrolipid mantle. This allows allergens to penetrate directly deep into the epidermis.
Sensitization is systemic in nature. Exacerbations are caused not only by contact. Allergens can enter via inhalation or through the gastrointestinal tract, where they are captured by mucosal dendritic cells, initiating a general immune response.
Morphology and risk factors
The transition to the chronic stage leads to structural changes in the epidermis. Clinically, this manifests as lichenification—skin thickening with accentuated skin markings. Pathomorphologically, a significant thickening of the stratum corneum is observed due to impaired natural apoptosis of keratinocytes.
The disease occurs when heredity and environmental triggers combine. Risk factors include:
- Antenatal: highly allergenic maternal diet, smoking, infections, gestation complications.
- Postnatal: operative delivery, early formula feeding, dysbiosis, and digestive disorders (malabsorption) in the child.
- Household: high concentration of aeroallergens and pollutants worsens the course of dermatitis.
Class and exam questions
What is the dualism of inflammation in atopic dermatitis?
The acute course is associated with IgE-dependent immediate-type reactions. Upon transitioning to a chronic course, a delayed-type allergic reaction joins in, with a predominance of Th1 cells and macrophages.
What role do Langerhans cells play?
These are antigen-presenting cells of the epidermis. They capture allergens, migrate to the dermis, and activate specific Th2 lymphocytes.
Why does the skin thicken during chronic progression?
The formation of lichenification and thickening of the epidermal stratum corneum occur due to impaired processes of natural apoptosis (programmed cell death) of keratinocytes.
Can an exacerbation begin without skin contact?
Yes, sensitization is systemic. Antigens can enter through the gastrointestinal tract or respiratory tract, where they are captured by mucosal dendritic cells, triggering an immune response.
What else to study on this topic
- Cytokine profile of the Th2 response (IL-4, IL-5, IL-13, TSLP)
- Mechanisms of leukocyte diapedesis into the dermis and epidermis
- Structural features of the skin hydrolipid mantle in normal states and in atopy
- Impact of pollutants on the continuous-relapsing course
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