Humoral immunity

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Humoral immunity is the aspect of

antimicrobial peptides – located in extracellular fluids. Humoral immunity is named so because it involves substances found in the humors, or body fluids. It contrasts with cell-mediated immunity
. Humoral immunity is also referred to as antibody-mediated immunity.

The study of the

cellular components that form the immune system, including their function and interaction, is the central science of immunology. The immune system is divided into a more primitive innate immune system and an acquired or adaptive immune system of vertebrates, each of which contain both humoral and cellular
immune elements.

Humoral immunity refers to antibody production and the coinciding processes that accompany it, including:

Th2 activation and cytokine production, germinal center formation and isotype switching, and affinity maturation and memory cell generation. It also refers to the effector functions of antibodies, which include pathogen and toxin neutralization, classical complement activation, and opsonin promotion of phagocytosis and pathogen elimination.[1]

History

The concept of humoral immunity developed based on the analysis of

Following the 1888 discovery of the bacteria that cause

antibodies form against the plant toxins ricin and abrin, and proposed that these antibodies are responsible for immunity.[2] Ehrlich, with his colleague von Behring, went on to develop the diphtheria antitoxin, which became the first major success of modern immunotherapy.[3] The discovery of specified compatible antibodies became a major tool in the standardization of immunity and the identification of lingering infections.[3]

Major discoveries in the study of humoral immunity[3]
Substance Activity Discovery
Alexin(s)/Complement(s) Soluble components in the serum
that are capable of killing microorganisms
Buchner (1890),
Ehrlich (1892)
Antitoxins
Substances in the serum that can neutralize the activity of toxins, enabling
passive immunization
von Behring and Shibasaburō (1890)
Bacteriolysins Serum substances that work with the
complement proteins to induce bacterial lysis
Richard Pfeiffer (1895)
Bacterial agglutinins
and precipitins
Serum substances that aggregate bacteria
and precipitate bacterial toxins
von Gruber and Durham (1896),
Kraus (1897)
Hemolysins Serum substances that work with complements
to lyse red blood cells
Jules Bordet (1899)
Opsonins Serum substances that coat the outer membrane of foreign substances and enhance the rate of phagocytosis by macrophages Wright and Douglas (1903)[4]
Antibody Original discovery (1900), antigen-antibody binding hypothesis (1938), produced by B cells (1948), structure (1972), immunoglobulin genes (1976) Ehrlich[2]

Antibodies

Immunoglobulins are glycoproteins in the immunoglobulin superfamily that function as antibodies. The terms antibody and immunoglobulin are often used interchangeably. They are found in the blood and tissue fluids, as well as many secretions. In structure, they are large Y-shaped globular proteins. In mammals there are five types of antibody: immunoglobulin A, immunoglobulin D, immunoglobulin E, immunoglobulin G, and immunoglobulin M. Each immunoglobulin class differs in its biological properties and has evolved to deal with different antigens.[5] Antibodies are synthesized and secreted by plasma cells that are derived from the B cells of the immune system.

An antibody is used by the acquired immune system to identify and neutralize foreign objects like bacteria and viruses. Each antibody recognizes a specific antigen unique to its target. By binding their specific antigens, antibodies can cause agglutination and precipitation of antibody-antigen products, prime for phagocytosis by macrophages and other cells, block viral receptors, and stimulate other immune responses, such as the complement pathway.

An incompatible

acute kidney failure
.

Antibody production

In humoral immune response, the B cells first mature in the bone marrow and gain B-cell receptors (BCRs) which are displayed in large numbers on the cell surface.[6]

These membrane-bound protein complexes have antibodies which are specific for antigen detection. Each B cell has a unique antibody that binds with an antigen. The mature B cells then migrate from the bone marrow to the lymph nodes or other lymphatic organs, where they begin to encounter pathogens.

Step 1: A macrophage engulfs the pathogen. Step 2: The macrophage then digests the bacterium and presents the pathogen's antigens. Step 3: A T helper cell binds to the macrophage and becomes an activated T helper cell. Step 4: The activated T helper cell binds to a B cell in order to activate the B cell. Step 5: When the B cells are activated, some B cells turn into plasma cells and are released in the blood, while other B cells become B memory cells that quicken response for a second exposure. Step 6: Plasma cells then secrete antibodies, which bind to antigens to fight the invading pathogens.

B cell activation

When a B cell encounters an antigen a signal is activated, the antigen binds to the receptor and is taken inside the B cell by

MHC-II proteins are recognized by helper T cells, stimulating the production of proteins, allowing for B cells to multiply and the descendants to differentiate into antibody-secreting cells circulating in the blood.[7] B cells can be activated through certain microbial agents without the help of T-cells and have the ability to work directly with antigens to provide responses to pathogens present.[7]

B cell proliferation

The B cell waits for a helper T cell (TH) to bind to the complex. This binding will activate the TH cell, which then releases cytokines that induce B cells to divide rapidly, making thousands of identical clones of the B cell. These daughter cells either become plasma cells or memory cells. The memory B cells remain inactive here; later, when these memory B cells encounter the same antigen due to reinfection, they divide and form plasma cells. On the other hand, the plasma cells produce a large number of antibodies which are released freely into the circulatory system.

Antibody-antigen reaction

These antibodies will encounter antigens and bind with them. This will either interfere with the chemical interaction between host and foreign cells, or they may form bridges between their antigenic sites hindering their proper functioning. Their presence might also attract macrophages or killer cells to attack and phagocytose them.

Complement system

The complement system is a

plasma membrane leading to cytolysis of the cell. The complement system consists of more than 35 soluble and cell-bound proteins, 12 of which are directly involved in the complement pathways.[1]
The complement system is involved in the activities of both innate immunity and acquired immunity.

Activation of this system leads to cytolysis,

Three biochemical pathways activate the complement system: the

mannose-binding lectin pathway. The classical complement pathway typically requires antibodies for activation and is a specific immune response, while the alternate pathway can be activated without the presence of antibodies and is considered a non-specific immune response.[1] Antibodies, in particular the IgG1 class, can also "fix" complement.

B cell activation is a large part of the humoral immune response.

These processes differ only in the process of activating C3 convertase,[8]

which is the initial step of complement activation, and the subsequent process are eventually the same, forming a structure called the membrane attack complex (MAC) on the bacterial cell wall to destroy the bacteria.

See also

References

  1. ^ .
  2. ^ (Full Text Version) Cambridge University Press
  3. ^ a b c d Gherardi E. The experimental foundations of Immunology Archived 2011-05-30 at the Wayback Machine Immunology Course Medical School, University of Pavia.
  4. ^ Hektoen, L. (1909). Opsonins and Other Antibodies. Science, 29(737), 241–248. http://www.jstor.org/stable/1634893
  5. .
  6. ^ Boundless (2016-05-26). "Humoral Immune Response". Boundless. Archived from the original on 2016-10-12. Retrieved 2017-04-15.
  7. ^ a b Charles A Janeway, Jr; Travers, Paul; Walport, Mark; Shlomchik, Mark J. (2001). "B-cell activation by armed helper T cells". Immunobiology: The Immune System in Health and Disease. 5th Edition.
  8. ^ Charles A Janeway, Jr; Travers, Paul; Walport, Mark; Shlomchik, Mark J. (November 21, 2001). "The complement system and innate immunity". Immunobiology: The Immune System in Health and Disease (5th ed.). New York: Garland Science – via www.ncbi.nlm.nih.gov.

Further reading