Cytokine and Lymphocyte Profiles in Dogs with Atopic Dermatitis after Allergen-Specific Immunotherapy

Abstract

Canine atopic dermatitis (cAD) is a chronic and recurrent inflammatory and pruritic skin disease in dogs. Currently, allergen-specific immunotherapy (ASIT) is the only identified disease-modifying intervention for allergic diseases. It decreases the symptoms triggered by allergens and prevents recurrence of the disease in the long-term. The aim of our research was to determine how immunotherapy changes the proportion of lymphocyte subsets in dog peripheral blood and the levels of cytokines secreted by these cells during therapy. ASIT was applied for 6 months. Blood samples for further analyses were collected from patients in the third and sixth month of immunotherapy. Six out of seven dogs receiving ASIT showed a positive effect. A reduction in cytokine levels (IL-13, TNF-α) in peripheral blood of cAD patients and changes in the number of specific T cell subpopulations—reduction of Tc cells (CD8+) and increase of activated T cells (CD3+CD25+)—confirmed the beneficial effect of the applied ASIT. In addition, a significantly higher percentage of Treg cells (CD4+CD25+FOXP3+) was noted in cAD patients before treatment compared to healthy dogs. After 3 months of therapy, the percentage of Tregs significantly decreased, and after 6 months, it increased significantly again.

Efficacy of short‐term combination of intralymphatic allergen immunotherapy and lokivetmab treatment in canine atopic dermatitis: A double‐blinded, controlled, randomised study

“…[8][9][10] In dogs, similar findings have been shown including an increase of Treg cells in peripheral blood 11,12 and interleukin (IL)-10 serum concentrations, 11 change in allergen-specific serum IgE and IgG concentrations, 13 and reduction of inflammatory plasma cytokine concentrations. 12 Allergen-specific immunotherapy (ASIT) typically consists of an induction and a maintenance phase. During the induction phase, the amount of injected allergens is increased gradually until immunological tolerance is reached.…”

“…In humans, the mechanism behind ASIT includes the induction of allergen-specific regulatory T (Treg) cells and their cytokines, induction of allergenspecific immunoglobulin (Ig)G4 concentrations and reduction of both the ratio of Th2/Th1 cytokines and serum allergen-specific IgE. [8][9][10] In dogs, similar findings have been shown including an increase of Treg cells in peripheral blood 11,12 and interleukin (IL)-10 serum concentrations, 11 change in allergen-specific serum IgE and IgG concentrations, 13 and reduction of inflammatory plasma cytokine concentrations. 12 Allergen-specific immunotherapy (ASIT) typically consists of an induction and a maintenance phase.…”

Depletion of T and B cells in lymphoid tissues of mice induced by oclacitinib, a Janus kinase inhibitor

“…However our previous studies found that the drug may have a more complex mechanism of action (Jasiecka-Mikołajczyk et al 2021). Considering the fact that T and B cells are involved in the pathophysiology of AD in dogs (Olivry et al 1999, Nuttall et al 2002, Schlotter et al 2011, Majewska et al 2022, the depletive effect of the drug toward these cells may contribute to the beneficial effects of OCL in the treatment of skin allergic diseases.…”

“…The inflammatory reaction in this disease is caused by an imbalance between Th2 and Th1 cells, resulting in activation of B cells, which are stimulated to produce IgE. Binding of allergen-specific IgE to mast cells causes degranulation of these cells and the secreted inflammatory mediators lead to inflammation (Majewska et al 2022).…”

Canine Models of Inflammatory Skin Diseases and Their Application in Pharmacological Research

“…As mentioned above, AD is a chronically relapsing inflammatory skin disease, and as such, an influx of activated white blood cells, especially T cells, is a hallmark of AD. For this reason, T cells and their derived cytokines and chemokines have been extensively modeled to gain insight into the local and systemic immune milieu of the disease (Bruet et al., 2015; Majewska et al., 2022; Rostaher et al., 2018, and Bauman et al., 2022).…”