Hormonal Regulation of the Immune Response
Immune responses do not exist in isolation: they develop against the background of hormonal regulation operating via a classical feedback loop. General metabolism is critically important for host defense. For example, marked metabolic disturbances can lead to thymus hypoplasia, which automatically causes weakened immunity and the development of immunodeficiency.
Depending on their vector of influence on the immune system, hormones are divided into two groups:
- Immunostimulants (activate defensive reactions): insulin, thyroxine (thyroid hormone), and somatotropin (growth hormone from the anterior pituitary). Growth hormone deficiency negatively affects immune status.
- Immunosuppressants (suppress defenses): glucocorticoids and all major sex hormones (androgens, estrogens, progesterone).
A striking clinical example of the link between the endocrine system and reactivity is diabetes mellitus. Patients with this condition have a sharply increased susceptibility to pyogenic infections. Immunodeficiency in diabetes is caused by three factors: a severe general metabolic disorder, the loss of the physiological stimulating effect of insulin on immunity, and direct suppression of phagocytosis.
Genetic Polymorphism and Resistance Mechanisms
Individual resistance of the organism is strictly genetically determined. Genes control not only protection against the initial onset of infection but also resistance to its progression. Furthermore, genetics determines the organism's ability to keep a pathogen in a latent state and shapes the phenomenon of specific resistance to particular phases of the microbial life cycle.
There are two main mechanisms for realizing genetic resistance:
- Via the immune system. This is primarily driven by the major histocompatibility complex (MHC) antigens. A huge role is played by mutations in genes directly responsible for the quality of phagocytosis, proper differentiation of T and B lymphocytes, and the synthesis of signaling molecules—cytokines (particularly interferons).
- Outside the immune system (metabolic defense). This mechanism targets highly specialized microbes that require strictly specific tissue substrates for nutrition and reproduction. If a genetic mutation alters the structure of such a substrate, the pathogen loses the ability to utilize it and dies without the direct participation of immune cells.
Host-Pathogen Interaction
The development of an infection is always a dynamic balance of forces. Factors that increase nonspecific resistance and immunity block the development of the pathological process. Conversely, any triggers that diminish host defenses promote the unimpeded spread and generalization of the infection.
Interaction between reactivity and the microbe has a crucial evolutionary aspect, as the macroorganism acts as an environment for strain selection:
- In an immunodeficient organism, defense is minimal, so the pathogen does not need to expend resources on adaptation or evasion. Under such hospitable conditions for the microbe, highly virulent strains capable of maximum aggressive replication are selected.
- In an immune (resistant) organism, the microbe must survive under the continuous pressure of defense systems. Aggressive individuals are rapidly eliminated, and therefore predominantly low-virulence strains that are forced to adapt to the powerful host response survive and are selected.