Cellular immunity and T-helper cells
T-lymphocytes play the primary role in the cellular mechanisms of specific defense. Upon antigen recognition, they differentiate into memory cells (for a rapid response upon re-exposure) and effectors, which include cytotoxic cells and T-helper cells (Th). T-helpers are divided into two subsets based on the chemical mediators they secrete—cytokines:
- Th1 cells secrete interleukin-2 (IL-2), interferon-gamma (IFN-$\gamma$), and tumor necrosis factor (TNF). They sustain inflammation, activate macrophages, and natural killer (NK) cells. This type of response is characteristic of acute infection and provides defense against intracellular protozoa.
- Th2 cells secrete IL-4, IL-5, and IL-10. They trigger humoral immunity by activating B cells. Th2 cells are associated with chronic infection, allergic manifestations, and are vital for the expulsion of intestinal helminths.
Humoral response and antibody functions
Humoral immunity is aimed at destroying extracellular forms of parasites (in the blood, body fluids, or intestinal lumen). The main mechanism is the production of specific antibodies (immunoglobulins) by B-lymphocytes.
Five classes of immunoglobulins participate in this defense:
- IgM — synthesized first. Their elevation is diagnostically significant in malaria and trypanosomiasis.
- IgG — function as antitoxins. Markers of malaria and visceral leishmaniasis.
- IgA — protect mucous membrane surfaces.
- IgD — function as receptors on B-lymphocytes.
- IgE — key participants in anti-parasitic defense and initiators of allergy.
Antibodies neutralize the pathogen (e.g., preventing Plasmodium merozoites from invading erythrocytes), prevent its spread during the acute phase, and bind the parasite's excretory-secretory products, forming immune complexes.
Eosinophils and mast cells
Parasitic infestations are classically accompanied by elevated eosinophil levels. Their destructive potential is realized via antibodies:
- Immunoglobulins (IgA, IgG, IgE) attach to the surface of the pathogen.
- Specific regions of these antibodies bind to eosinophil receptors.
- This triggers eosinophils to release lysosomal hydrolases and other cytotoxic factors that destroy the parasite.
Another important mechanism involves mast cells and type I hypersensitivity (immediate hypersensitivity). There is little free IgE circulating in the blood because these antibodies are adsorbed onto the surface of mast cells. Upon re-exposure to the antigen, a reaction occurs, causing mast cells to degranulate and release active substances, which can lead to the classic clinical picture of immediate hypersensitivity—anaphylactic shock.
Influence of genetics and host status
The severity of parasitic infections directly depends on the status of the host organism. In non-immune travelers, pregnant women, or children with protein deficiency, infections (e.g., pneumocystosis or amebiasis) are significantly more severe. In immunodeficiencies (including HIV), reactivation of latent infections is characteristic: toxoplasmosis affects the CNS and lungs, and visceral leishmaniasis takes a malignant course.
At the same time, host genetic mutations can serve as protection. Examples of genetic resistance to malaria include:
- Absence of Duffy antigens: renders indigenous populations of West Africa completely resistant to Plasmodium vivax.
- Hemoglobinopathies (HbS, HbC, HbE): prevent the development of severe clinical manifestations.
- G6PD deficiency and thalassemia: reduce mortality from falciparum malaria.
Immunity in helminthiases
While lasting immunity can form in trypanosomiasis or leishmaniasis, infection with worms (enterobiasis, ascariasis) induces a relative (non-sterile) immunity. This means the individual is not protected against reinfection.
Helminths successfully establish chronicity through their survival mechanisms: potent immunosuppressive properties, loss of target receptors, and antigenic mimicry (where their molecules resemble host tissues). Clinically, this is accompanied by hepatosplenomegaly, and immunological shifts are observed primarily during the migration of the larval stage.
Briefly: answers to topical questions
What specific cytotoxic proteins do eosinophils release during degranulation to destroy helminths?
During degranulation, eosinophils release four major granule proteins involved in macroparasite damage: major basic protein (MBP), eosinophil cationic protein (ECP), eosinophil peroxidase (EPO), and eosinophil neurotoxin (EDN). Upon secretion, MBP converts into a soluble form and disrupts the membrane integrity of helminth cells. MBP, ECP, EPO, and EDN can all damage macroparasite cells.
What fractions and pathways of the complement system are involved in parasite lysis?
The complement system participates in parasite lysis. Cleavage products of the C3 component, primarily C3b, provide opsonization, while the membrane attack complex causes target cell cytolysis. Activation can be initiated via the classical, alternative, or lectin pathways. The phase of target cell lysis is identical for all three pathways; at the initial stage of the immune response, complement activation occurs predominantly via the alternative pathway.
Which cells act as the primary antigen-presenting cells (APCs) during the initial recognition of parasite antigens?
Macrophages and dendritic cells participate in antigen presentation: macrophages present antigens to T-lymphocytes, while dendritic cells present them to CD4+ T-lymphocytes. Eosinophils are also capable of acting as antigen-presenting cells as they express MHC class I and II molecules.
To remember the direction of the response: Th1 — intracellular (protozoa), Th2 — extracellular (helminths and allergy).
Class and exam questions
Why are immune complexes dangerous in parasitic infections?
Antibodies frequently react with substances secreted by the parasite, forming antigen-antibody complexes. Circulating in the bloodstream and depositing in tissues, they can cause internal organ dysfunction.
Does lifelong immunity develop after recovery?
In certain diseases (e.g., leishmaniasis), lasting immunity is formed. However, in helminthiases, immunity is relative and does not protect against reinfection.
What else to study on this topic
- The mechanism of antigenic mimicry in helminths
- Pathogenetic features of latent toxoplasmosis reactivation in HIV-infected patients
- The role of the complement system in enhancing phagocytosis
- Causes of high levels of non-specific antibodies during parasitic infections
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