Alecu Mihail MD, PhD

Alecu Mihail MD, PhD
Clinical Hospital for Infectious and Tropical Diseases “Dr. Victor Babeş “Bucharest
“Titu Maiorescu” University of Medicine, Bucharest

Innate immunity in autoimmune and inflammatory skin diseases
Authors: Mihail Alecu, Gabriela Coman, Ionica Rădulecu, Alina Muşetescu, Andreia Oana Coman, Mirela Sfârâială Luculescu

The innate immunity is one of the two aspects of general immunity, and it is also the first line of defense against pathogens. It is the immunity one is born with, it is fast, non-specific, without memory and independent of the nature of the antigen. The main mechanism of action consists in the expression on the surface of several cells (keratinocytes, NK cells, dendritic cells, monocytes, macrophages) of a toll-like protein family that recognize a molecular pattern on the surface of a microbial pathogen. Activation of these receptors induces a transduction signal that produces the activation of transcription factors (NFkB) with the production of TNF, IL1, IFNγ and ROS. These cytokines are directly or indirectly involved in pathogen destruction, inflammatory cell activation, induction of tissue restoration, mobilization and activation of the constituent cells of the adaptive immune system response.
Keratinocytes, NK cells, dendritic cells, monocytes, macrophages express transmembrane proteins on their surface, which are members of the TLR family, so these cells participate in both the destruction of pathogenic germs and other processes, such as inflammation, activation of specific immunity, being the basis for diseases such as lupus erythematosus, pemphigus vulgaris, psoriasis.
In the pathogenesis of systemic lupus erythematosus, the massive implication of innate immunity has been demonstrated, so both nucleic acids resulting from cellular destruction and circulating immune complexes can activate TLR receptors (TLR7 and TLR9) that are found to be excessively expressed on mononuclear cells in the blood. Also, TLR 7 and TLR9 are involved in autoantibody production, and TLR 2 and TLR 4 are involved in regulating the activity of dendritic cells and Th17 lymphocytes in IL17 production. In pemphigus vulgaris, an increase in TLR4 expression in keratinocytes was seen in both the basal layer and the upper epidermal layers. In psoriasis, keratinocytes excessively express TLR1, TLR2 and TLR5, with significant differences between normal skin and lesional skin. The keratinocyte from injured skin, TLR receptor-activated (TLR2, TLR3, TLR4) increases the production of TNF alpha, IL8 and other proinflammatory cytokines. Activation of innate and adaptive immune response leads to the activation of T ymphocytes, Th1 and especially Th17 lymphocytes, with excess IL17 production. Excessive proinflammatory cytokines as well as the action of LL37 peptide induces excessive proliferation of keratinocytes.
Highlighting the implication of innate immunity in cutaneous pathology opens new perspectives on understanding the pathogenic processes that underlie several types of skin disorders, especially in the initiation phase of these processes.

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