Innate immunity receptors
Innate immunity relies on genetically determined receptors, numbering only a few dozen. Their main task is to detect PAMPs (pathogen-associated molecular patterns) characteristic of microorganisms.
- On the cell surface: Toll-like receptors (TLRs) and lectin receptors function here.
- Inside cells: NOD-like and other cytosolic receptors are responsible for detecting intracellular threats.
- In tissue fluids: Soluble molecules, such as complement components and pentraxins, also perform a receptor function by binding to pathogens and acting as opsonins.
It is important to note that without primary stimulation of these pattern-recognition receptors, the initiation of adaptive immunity is impossible.
Adaptive immunity receptors
The adaptive response is characterized by high specificity, which is achieved through unique antigen-recognition receptors on lymphocytes.
- TCR (T-cell receptor): Is unable to "see" free antigen. It recognizes only those peptides that have been processed and displayed on the surface of other cells in a complex with major histocompatibility complex (MHC) molecules. Recognition occurs in regional lymph nodes and serves as the moment the immune response is turned on.
- BCR (B-cell receptor): Unlike the TCR, it recognizes free viral antigens, extracellular viruses, or fragments of destroyed cells (detritus). The soluble form of these receptors is antibodies, which are secreted by plasma cells and can neutralize antigens or recruit phagocytes.
Role of MHC molecules in receptor interactions
MHC molecules are a crucial link, without which antigen recognition by T lymphocytes is impossible.
- MHC-I: incorporate peptide fragments (including viral ones) and present them for recognition by CD8+ T cell receptors. The loss of MHC-I by an infected cell serves as a signal for its destruction by natural killers.
- MHC-II: Expressed on antigen-presenting cells (APCs), such as dendritic cells and macrophages. Essential for presenting peptides to CD4+ T-helper cell receptors. MHC-II expression is dramatically enhanced by interferon-gamma (IFNγ).
Cellular stress receptors
Receptors that respond to changes in the state of the body's own cells play a special role in antiviral defense.
The key molecule here is NKG2D. This activating receptor is expressed on NK (natural killer) cells and NKT cells. It recognizes stress proteins that appear on the surface of infected cells.
Upon recognizing stress, NKT cells synthesize IFNγ, which serves as an additional stimulus for NK cells. If the target cell has simultaneously lost MHC-I, NK cells perform its cytolysis as part of innate immunity.
Receptor apparatus of "non-professional" immunocytes
Innate immunity is able to enlist vascular endothelial and epithelial cells in defense. At rest, they carry TLRs (e.g., TLR-2 and TLR-4) to recognize PAMPs, and constitutively (spontaneously) express receptors for proinflammatory cytokines (IL-1, TNFα, IL-6, IL-8).
Upon cytokine binding, new receptors appear on these cells, giving them macrophage-like properties:
- Fcγ receptors and complement receptors—provide phagocytic capability.
- Adhesion receptors (selectins, ICAM-1, ICAM-3)—help interact with other cells.
- MHC-II and costimulatory molecules (CD40, CD80, CD86)—allow them to function as APCs for memory cells.
Although these properties are less pronounced than in professional macrophages, they significantly expand the body's defense potential. After inflammation resolves, cells lose these receptors and return to normal.
Remember the receptor-target pairs: TLRs search for microbial patterns (PAMPs), TCRs check cell "passports" (MHCs), and BCRs catch free antigens.
Class and exam questions
How do T lymphocytes recognize a virus?
Via the cellular TCR receptor, which reads the viral peptide only if it is embedded in an MHC molecule on the surface of an antigen-presenting cell.
What causes NK cells to destroy the body's own cells?
The signal for attack is the recognition of stress proteins via the NKG2D receptor against the background of the target cell's loss of MHC-I molecules.
Can epithelial cells perform macrophage functions?
Yes, under the influence of cytokines, they begin to express Fcγ receptors for phagocytosis and MHC-II molecules for antigen presentation, although they do this more weakly than professional immunocytes.
What else to study on this topic
- Antigen processing and presentation by dendritic cells
- Mechanisms of CD8+ T-lymphocyte cytotoxicity
- Role of interferon-gamma (IFNγ) in immune integration
- Stages of phagocytosis and intracellular pathogen destruction
- Formation of immunological memory and secondary immune response
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Other topics in the "Innate Immunity" section
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