Recognition and Activation Mechanisms
Adaptive immunity is mediated by specialized cells—T lymphocytes and B lymphocytes. They are capable of precisely recognizing virtually any peptide antigen due to unique antigen-recognition receptors on their surface:
- TCR (T-cell receptor) on T lymphocytes.
- BCR (B-cell receptor) on B lymphocytes.
There is a strict division of labor in the adaptive immune system. T lymphocytes are responsible for the cell-mediated component of the immune response. Conversely, B lymphocytes are responsible for the humoral component, synthesizing specific antibodies. A key feature of these cells is that they must undergo additional differentiation to fully initiate protective functions and transition into an active state.
Classification by Mode of Acquisition
Depending on how the body acquires protection, adaptive immunity is broadly divided into two forms:
- Active immunity. Formed by the host's own immune system in response to antigen exposure. It can be post-infectious (arising after a natural infection) or post-vaccination (induced by targeted administration of vaccines).
- Passive immunity. The host does not synthesize protection independently, but receives preformed antibodies from an outside source. This form can be natural, when maternal IgG antibodies are transferred to the fetus across the placenta (transplacentally), protecting the newborn. There is also artificial passive immunity, achieved through the medical administration of immune sera or readymade immunoglobulin preparations.
Classification by Pathogen Presence and Scale
Based on the clearance of the pathogen from the body, immunity can be:
- Sterile. Resistance persists even after the pathogen's antigens have been completely eliminated from body tissues and fluids.
- Non-sterile. Protection is maintained only as long as the infectious agent physically persists within the body. A classic clinical example of this state is immunity in tuberculosis.
Based on its distribution, immunity is divided into systemic (generalized), which encompasses the entire body, and local, which increases resistance only in specific tissues or organs. A key example of a local response is mucosal immunity—a complex of protective mechanisms operating at the level of mucosal membranes.
Target Specificity of the Immune Response
Depending on the main target, immunity can be antitumor, transplantation-related, or anti-infective. Anti-infective immunity, in turn, has strict specificity based on the attacking pathogen type:
- Antiviral
- Antibacterial
- Antifungal
- Antiprotozoal (directed against protozoan organisms)
Differences from Innate Immunity
While adaptive immunity requires contact with an antigen and time for differentiation, innate immunity relies on baseline molecular mechanisms for pathogen recognition and stress response.
The innate arm features coordinated mechanisms:
- Cellular mechanisms: macrophages and neutrophils cooperate to engulf and digest foreign particles (phagocytosis) and destroy target cells (cytolysis).
- Humoral mechanisms: blood plasma proteins (e.g., the complement system and C-reactive protein) react instantly to carbohydrate components of microbial cell walls. Innate immune cells can also synthesize various active effector molecules to combat threats.