Pattern (group) recognition
Group recognition forms the basis of innate immunity. Its primary task is to identify conserved molecular structures characteristic of entire groups of pathogens (pathogen-associated molecular patterns).
This mechanism evolved through phylogenesis, so discrimination between 'self' and 'non-self' here is absolute. Receptors are hardwired from the start to recognize only foreign molecules and ignore the host's own tissues. These include TLRs, NLRs, CLRs, RIGs, DAI, soluble receptors, and Scavenger receptors.
The genes encoding these receptors are strictly determined. Consequently, all cells within a population (predominantly of the myeloid lineage, but also any other nucleated cells) carry an identical set of sensors on their surface. The response to a threat occurs immediately, without the need for additional co-stimulatory signals. However, immunological memory does not develop in this process: every new encounter with a pathogen is handled by the immune system as if it were the first.
Antigenic (individual) recognition
Individual recognition is the prerogative of adaptive immunity, represented by B and T lymphocytes. The targets here are specific antigenic epitopes. They can be found either as part of free molecules or presented in complex with MHC molecules.
The specificity of such receptors (BCR on B cells, TCR-γδ and TCR-αβ on T cells) is not initially encoded in the genome. It is formed entirely at random during the differentiation of each individual lymphocyte in ontogenesis. Due to this, the distribution of receptors is clonal: each lymphocyte clone recognizes only its specific antigen.
For a full-fledged immune response, simple binding to an antigen is insufficient—co-stimulation is strictly required. Developing such a reaction takes time, but the clonal organization principle enables the formation of immunological memory.
The problem of randomness and autoimmunity
Because the antigen-recognition receptors of adaptive immunity are generated randomly, clones targeting the body's own structures inevitably arise.
To prevent self-destruction, additional selection mechanisms are required. Their role is to identify and destroy autoreactive, 'dangerous' lymphocytes. Nevertheless, this discrimination is imperfect. If selection mechanisms fail, the surviving 'unwanted' clones can trigger autoimmune processes—aggressive reactions against self-antigens that lead to host tissue damage.
Interplay between innate and adaptive immunity
Both types of recognition do not work in isolation, forming an integrated defense system of the organism.
- Foundation: Innate immunity serves as the baseline for adaptive immunity. Lymphocytes can recognize an antigen only through presentation, which is carried out primarily by innate immune cells.
- Effector phase: The direct elimination of the antigen and the cells bearing it is mediated by innate immunity mechanisms. However, thanks to the adaptive branch, these baseline reactions acquire a specific component—strict targeting toward a specific antigen, which dramatically increases their efficacy.
Briefly: answers to topical questions
Which cells act as antigen-presenting cells to trigger the adaptive response?
Dendritic cells, macrophages, and B lymphocytes act as 'professional' antigen-presenting cells. Dendritic cells are critically important specifically for initiating the primary immune response.
- Dendritic cells efficiently activate naive T cells and trigger the primary response.
- Macrophages activate effector T cells and memory cells.
- B lymphocytes activate helper T lymphocytes.
There are also 'non-professional' antigen-presenting cells (such as endothelial and epithelial cells) that can acquire these properties when activated under inflammatory conditions.
With which classes of MHC molecules are antigens presented to T helper cells and cytotoxic T lymphocytes?
Antigens are presented to T lymphocytes in complex with major histocompatibility complex (MHC) class I or class II molecules, depending on the cell type.
| T lymphocyte type | MHC molecule class | Coreceptor |
|---|---|---|
| T helper cells | MHC-II | CD4 |
| Cytotoxic T lymphocytes | MHC-I | CD8 |
Recognition of the MHC-antigen complex is a prerequisite for T cell activation, with co-receptors ensuring affinity for specific MHC classes.
What types of selection do lymphocytes undergo to prevent autoimmune reactions?
To prevent autoimmune reactions, lymphocytes undergo negative selection, aimed at eliminating autoreactive clones.
- Negative selection of B lymphocytes takes place in the bone marrow, spleen, and lymph nodes, ensuring the elimination of autospecific B cells upon responding to a autoantigen.
- Negative selection of T lymphocytes occurs in the thymus, where developing thymocytes interact with stromal cells. Upon recognizing self-antigens, autoreactive clones are destroyed via apoptosis.
T cells also undergo positive selection and β-selection, but it is negative selection that limits aggressiveness against self-molecules.
What specific molecular patterns (PAMPs) are recognized by innate immunity receptors?
Innate immunity receptors recognize conserved structures of microorganisms—pathogen-associated molecular patterns (PAMPs).
The main types of PAMPs include:
- Lipopolysaccharides (LPS), characteristic of Gram-negative bacteria.
- Lipoteichoic acids, present in Gram-positive microorganisms.
- Peptidoglycans, components of the bacterial cell wall.
- Teichoic acids, recognized by membrane receptors.
- Zymosan and lipoarabinomannan, exogenous ligands for membrane receptors.
- DNA of bacterial origin.
- RNA of viral origin.
These structures are stable, change little during evolution, and are unequivocally associated with microbial pathogenicity.
Which molecules provide the co-stimulatory signal during lymphocyte activation?
The co-stimulatory signal during lymphocyte activation is provided by the paired interaction of molecules on the surface of antigen-presenting cells (APCs) and T lymphocytes.
The main activating co-stimulation pathways:
- CD80 (B7-1) and CD86 (B7-2) are ligands on the surface of APCs (dendritic cells, macrophages, B cells) that bind to the CD28 receptor on T cells.
- ICOSL is a ligand on APCs that interacts with the ICOS receptor on T lymphocytes.
Signal transmission via these molecules complements the specific signal from the T-cell receptor and is a mandatory condition for full T-cell activation; lack of co-stimulation leads to anergy.
To avoid confusing the types of recognition: Pattern recognition is like a standard fire alarm (triggers immediately for everyone in the same way, reacts to smoke, genetically built-in). Antigenic recognition is like an eye retina scanner (individual, takes time to verify the profile, but 'remembers' the intruder).
Class and exam questions
Why doesn't innate immunity cause autoimmune diseases?
Its receptors were formed in phylogeny and are genetically programmed to recognize only foreign conserved molecules, so the self-nonself discrimination is perfect.
Can antigenic epitopes be recognized in a free state?
Yes, but only by specific receptors (e.g., B lymphocytes). In other cases, epitopes must be embedded in MHC molecules for presentation.
What does clonal distribution of receptors mean?
This is a principle of adaptive immunity where each individual lymphocyte clone carries unique receptors on its surface that react to only one strictly defined antigen.
What else to study on this topic
- Structure and functions of pattern recognition receptors (TLRs, NLRs, CLRs, RIGs, DAIs).
- Mechanisms of antigen presentation in complex with MHC molecules.
- Stages and mechanisms of lymphocyte clone selection in ontogeny.
- The role of costimulation in the activation of the adaptive immune response.
- Interaction of innate immune effector mechanisms with specific components.
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