User:Judgementkazzy822/Humoral immunity

Article Draft

The following are my edits for the Humoral Immunity wikipedia page. There are 3 new citations, and edits to the antibodies, antibody production, and complement system sections. My edits are in BOLD.

The original article is linked here: Humoral immunity

On a separate sandbox I'm working on adding some more citations and an image to add for the complement system for the different pathways.

Feel free to let me know what edits I can make to improve!

Antibodies

Main article: Antibody

Antibodies or Immunoglobulins are glycoproteins found within blood and lymph. Structurally, antibodies 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. 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 blood transfusion causes a transfusion reaction, which is mediated by the humoral immune response. This type of reaction, called an acute hemolytic reaction, results in the rapid destruction (hemolysis) of the donor red blood cells by host antibodies. The cause is usually a clerical error, such as the wrong unit of blood being given to the wrong patient. The symptoms are fever and chills, sometimes with back pain and pink or red urine (hemoglobinuria). The major complication is that hemoglobin released by the destruction of red blood cells can cause acute kidney failure.

Antibody production

In humoral immune response, the naive B cells begin the maturation process in the bone marrow, gaining B-cell receptors (BCRs) along the cell surface. These BCRs are membrane-bound protein complexes that have a high binding affinity for specific antigens; this specificity is derived from the amino acid sequence of the heavy and light polypeptide chains that constitute the variable region of the BCR. Once a BCR interacts with an antigen, it creates a binding signal which directs the B cell to produce a unique antibody that only binds with that 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 endocytosis. The antigen is processed and presented on the B cell's surface again by MHC-II proteins. The 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. 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.

B cell proliferation

The B cell waits for a helper T cell (T_H) to bind to the complex. This binding will activate the T_H 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 natural killer cells to attack and phagocytose them.

Complement system

Main article: Complement system

Three biochemical pathways activate the complement system: the classical complement pathway, the alternate complement pathway, and the mannose-binding lectin pathway. These processes differ only in the process of activating C3 convertase, which is the initial step of complement activation, and the subsequent process are eventually the same. The classical pathway is initiated through exposure to free-floating antigen-bound antibodies. This leads to enzymatic cleavage of smaller complement subunits which eventually synthesize to form the C3 convertase.

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

This differs from the mannose-binding lectin pathway which, as the name suggests, is initiated by bacterial carbohydrate motifs, such as mannose, found on the surface of bacterium. After the binding process, the same subunit cleavage and synthesis occurs like in the classical pathway. The alternate complement pathway completely diverges from the previous pathways, as this pathway spontaneously initiates in the presence of hydrolyzed C3, which then recruits other subunits which can be cleaved to form C3 convertase. In all three pathways, once C3 convertase is synthesized, complements can be cleaved into subunits which either form a structure called the membrane attack complex (MAC) on the bacterial cell wall to destroy the bacteria or act as cytokines and chemokines, amplifying the immune response.