Immunity, innate

System of congenital, humoral (alternative complement activation; antimicrobial peptides) and cellular defense mechanisms (e.g. macrophages) that are activated in the early phase of defense against an invading pathogen. It thus represents a significant part of the immune system and, in the absence of acquired or adaptive immunity, enables the defence against microorganisms that threaten the integrity of the organism.

The innate immune system can be divided into two main components:

1. into a secretory component: antimicrobial peptides, complement factors, acute phase proteins (e.g. C-reactive protein).

2. into cellular components and pathogen recognition receptors (PRRs).

Among the best known PRRs are the Toll-like receptors. These recognize PAMPs (pathogen associated molecular patterns) on the cell surface or in vesicles of the cells. Intracellularly invaded pathogens are not detected by membrane-bound receptors but by cytosolic receptors. These include:

• the "Retinoic acid-inducible gene I (RIG-I)-like receptors".
• the NOD-like receptors (nucleotide-binding oligomerization domain like receptors, also called NLRs).

For the recognition of the very heterogeneous and large group of pathogens, only a limited number of genetically determined receptors, PRRs (see below Pattern Recognition Receptor) are available. An essential principle of innate immunity is not to recognize every possible antigen, but only a few highly conserved antigenic structures. These antigenic structures are called "pathogen associated molecular patterns" ( PAMPs ).

Principle: An invading pathogen is recognized by the organism as "foreign" via PRRs. This leads to the activation of intracellular signal transduction cascades (damage asociated-molecular patterns - DAMPs -), among which the NFkappaB pathway plays an important role. This leads to the transcription of genes that transcribe inflammatory (TNF-alpha, IL-6, IL-12, etc.) but also anti-inflammatory cytokines (note: anti-inflammatory cytokines such as IL-10 lead to the fact that the inflammatory reaction can be terminated again and is not perpetuated). Furthermore, the pathogen is combated with the help of tissue macrophages, neutrophil and eosinophil granulocytes, NK cells and dendritic cells, antimicrobial peptides (AMPS), the complement system and the immune system.

Antimicrobial peptides play an important role in atopic eczema. In contrast to patients with psoriasis in whom an increased expression of cathelicidin and beta-defensin could be found, the upregulation of these AMPs is reduced in atopic eczema. One explanation for this is that their induction is inhibited by the Th2-cytokines IL-4 and IL-13, which also explains the secondary colonization of the skin of patients with atopical eczema.

1. Averbeck M et al (2007) Immunological basics of allergies. JDDG 5: 1015-1028
2. Volz T et al. (2015) On the role of the innate immune system in atloptic dermatitis. Dermatologist 66: 90-95