Reasons for the development of immunodeficiency states

  1. infections
  2. Autoimmune diseases
  3. Medications (corticosteroids, immunosuppressants, cytostatics), radiotherapy
  4. Endocrine diseases (obesity, diabetes)
  5. neoplasia
  6. stress
  7. Surgery (especially splenectomy)
  8. Protein loss (burn disease, chronic renal failure, enteropathy)
  9. nutritional deficiency
  10. Impact of adverse environmental factors

Viral infections

Viral infections with immunosuppressive potential: HIV, EBV infection, measles, CMVI, viral hepatitis

IDS formation mechanism: direct cytopathogenic potential of viruses, death of highly specialized regulatory cells, impaired function of infected cells.

IS target cells in some viral infections

IC cells Virus Outcome of the relationship between virus and cell
B-lymphocytes VEB Transformation of B-lymphocytes, their polyclonal activation, lymphoproliferative syndrome
T-lymphocytes measles virus Virus replication in T-lymphocytes, anergy
Type I T-cell leukemia virus T-cell lymphoma/leukemia
Human immunodeficiency virus type 1 and 2 Acquired immunodeficiency syndrome (AIDS)
Macrophages Dengue virus Marburg-Ebola virus Viral hemorrhagic fever

In most viral infections, predominantly T-cell immunodeficiency is formed. Immunodeficiency in this case can last from several weeks (influenza) to several months (measles, hepatitis B) and even years (infectious mononucleosis). With HIV infection, immunological disorders gradually progress and become the cause of death of the patient.

Some viruses have the ability to cause defects in neutrophilic granulocytes, reduce their bactericidal and digestive activity (influenza virus, MS, varicella zoster), which increases the risk of bacterial complications (otitis media, sinusitis, pneumonia).

The role of EBV in the formation of acquired hypogammaglobulinemia – CVID is discussed.

Bacterial infections

Bacterial infections with immunosuppressive potential: tuberculosis, brucellosis, syphilis, leprosy. They cause incomplete phagocytosis, a decrease in T-cell immunity. Secondary immunodeficiencies are detected in convalescents of severe bacterial infections (sepsis, meningitis, osteomyelitis).

Chronic bacterial infections contribute to the depletion of innate immunity factors, antibodies.

Fungal infections

Almost all mucocutaneous and visceral mycoses occur against the background of insufficient T-cell immunity and/or deficiency of phagocytic cells. The progression of fungal infections can cause further suppression of immune functions.

Exogenous deficiency of proteins, vitamins, microelements

Malnutrition is still the most common cause of immunodeficiency disorders in the world. In malnourished individuals, the incidence of infectious diseases is increased.

Micronutrient deficiency

Zinc and iron deficiencies often cause T-cell immunodeficiency. Magnesium deficiency can cause a decrease in the number of NK cells, disrupt the processes of adhesion and interaction of immunocompetent cells. Selenium deficiency leads to the formation of T-cell deficiency. Selenium is an important antioxidant; its deficiency can cause various disorders of innate and adaptive immunity.

Protein starvation leads to a deficiency of immunoglobulins, proteins of the complement system, proteins of the acute phase of inflammation. In young children, protein deficiency leads to thinning of the thymus cortex.

Protein loss

Loss of protein in the urine in nephrotic syndrome leads to hypoproteinemia and a decrease in serum immunoglobulins – IgG and IgA. IgM is not lost due to the larger molecule size. Secretory IgA decreases slightly, since most of it is located on the surface of the mucous membrane.

Protein loss can occur in enteropathies , inflammatory bowel disease, Crohn’s disease. In these cases, there is a decrease in both IgG and secretory IgA.

burn disease

Mechanisms for the development of IDS:

  1. damage to border tissues (violation of the barrier functions of the skin and mucous membranes),
  2. powerful stress,
  3. increased antigenic load due to denatured and dehydrated tissue proteins and enzymatic tissue autolysis,
  4. intense loss of immunoglobulins from plasma.

At stage 1, due to the loss of immunoglobulins, B-cell immunodeficiency develops with increased sensitivity to bacterial infections. Secondary T-cell deficiency occurs with a significant area of burn damage (more than 30% of the skin surface). Against the background of burns, there may be a decrease in the function of neutrophils, loss of immunoglobulins and complement components, T-cell deficiency. The consequence of this is the addition of infections.

Tumor diseases

An increased risk of developing infections is observed in patients with lymphoproliferative diseases. In patients with chronic lymphocytic leukemia, there is a decrease in immunoglobulins, which contributes to the development of respiratory infections, the severity of which increases as the disease progresses.

Patients with non-Hodgkin’s lymphomas often have severe impairment of cellular and humoral immunity.

In patients with melanoma, the risk of developing infectious complications increases 100 times. Even before chemotherapy in this group of patients, the humoral link of immunity was significantly suppressed.

The high frequency of opportunistic infections in the development of neoplasia is a consequence of both the immunosuppressive effect of the tumor itself and the ongoing chemotherapy.

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