"Immunity" - what is it, definition of the term
The term denotes an organism’s intrinsic capacity to detect, neutralize, and eliminate invading agents—including ectoparasites such as ticks, insects, lice, and fleas—through coordinated cellular and humoral mechanisms that prevent infection, limit tissue damage, and promote recovery.
Detailed information
Protective resistance against arthropod vectors such as ticks, true bugs, lice, and fleas involves multiple layers of host defense. The first line of defense consists of physical and chemical barriers that deter attachment and feeding. Skin integrity, sebum secretion, and hair distribution create an environment less favorable for colonization. When a parasite breaches these barriers, innate cellular mechanisms activate rapidly.
Macrophages, neutrophils, and dendritic cells recognize conserved molecular patterns on arthropod saliva and cuticle components. Pattern‑recognition receptors trigger cytokine release, which promotes inflammation and recruits additional effector cells. This response limits the duration of blood meals and reduces pathogen transmission.
Adaptive components generate specificity. B‑cell activation leads to the production of antibodies that bind vector salivary proteins, neutralizing their immunomodulatory effects. T‑cell subsets, particularly Th1 and Th17, produce interferon‑γ and IL‑17, enhancing macrophage microbicidal activity and strengthening barrier function. Memory cells ensure a faster, more robust reaction upon re‑exposure.
Key factors influencing the effectiveness of host resistance include:
- Genetic variation in major histocompatibility complex alleles that affect antigen presentation.
- Prior exposure history, which shapes the repertoire of memory B and T cells.
- Age and nutritional status, which modulate the overall capacity of the immune system.
- Co‑infection with other pathogens that can divert or suppress defensive pathways.
Vector‑derived molecules often target host defenses. Tick saliva contains anticoagulants, anti‑inflammatory agents, and complement inhibitors that suppress early inflammatory signals. Some bugs inject protease inhibitors that interfere with cytokine signaling. Lice secrete enzymes that degrade skin lipids, facilitating attachment. Flea saliva includes components that dampen neutrophil recruitment. Understanding these interactions guides the development of vaccines and therapeutics that enhance host resistance by blocking vector immunosuppression.
Effective control strategies integrate host‑focused approaches—such as immunization with recombinant salivary proteins—and vector management, including acaricides and environmental sanitation. By targeting both the biological mechanisms of resistance and the arthropod’s capacity to evade them, the overall burden of vector‑borne diseases can be reduced.