An antibody (Ab), also known as an immunoglobulin (Ig), is a large Y-shaped protein produced by B-cells that is used by the immune system to identify and neutralize foreign objects such as bacteria and viruses. The antibody recognizes a unique part of the foreign target, called an antigen.
Each tip of the “Y” of an antibody contains a paratope (a structure analogous to a lock) that is specific for one particular epitope (similarly analogous to a key) on an antigen, allowing these two structures to bind together with precision. Using this binding mechanism, an antibody can tag a microbe or an infected cell for attack by other parts of the immune system, or can neutralize its target directly (for example, by blocking a part of a microbe that is essential for its invasion and survival).
The production of antibodies is the main function of the humoral immune system.
Antibodies are produced by a type of white blood cell called a plasma cell.
… Soluble antibodies are released into the blood and tissue fluids, as well as many secretions to continue to survey for invading microorganisms.
Antibodies are glycoproteins belonging to the immunoglobulin superfamily; the terms antibody and immunoglobulin are often used interchangeably.
… Five different antibody isotypes are known in mammals, which perform different roles, and help direct the appropriate immune response for each different type of foreign object they encounter.
Though the general structure of all antibodies is very similar, a small region at the tip of the protein is extremely variable, allowing millions of antibodies with slightly different tip structures, or antigen binding sites, to exist. This region is known as the hypervariable region. Each of these variants can bind to a different target, known as an antigen.
This enormous diversity of antibodies allows the immune system to recognize an equally wide variety of antigens.
The large and diverse population of antibodies is generated by random combinations of a set of gene segments that encode different antigen binding sites (or paratopes), followed by random mutations in this area of the antibody gene, which create further diversity.
Antibody genes also re-organize in a process called class switching that changes the base of the heavy chain to another, creating a different isotype of the antibody that retains the antigen specific variable region. This allows a single antibody to be used by several different parts of the immune system.
What is an antinuclear antibody?
Anti-nuclear antibodies (ANAs, also known as anti-nuclear factor or ANF) are autoantibodies directed against contents of the cell nucleus.
They are present in higher than normal numbers in autoimmune disease. The ANA test measures the pattern and amount of autoantibody which can attack the body’s tissues as if they were foreign material. Autoantibodies are present in low titers in the general population, but in about 5% of the population, their concentration is increased, and about half of this 5% have an autoimmune disease.
What determines which antibodies are produced?
Enhancer genes regulate antibody production by a mechanism not yet completely understood.
… Enhancer genes control the reshuffling of antibody genes that makes a precise and coordinated attack possible.
Once your plasma white blood cells make a particular antibody, do they ever stop making it?
Not sure yet…. But…
Suppressor T cells:
A subset of T cells that turn off antibody production and other immune responses.
What regulates this?
In healthy individuals, the masses of cells that gather at an infected or injured site in the body produce factors that help fight off the infection. This process causes some inflammation and injury of healthy tissue, but usually the immune system possesses other factors that help to control this inflammatory process. In individuals with lupus, both B cells and T cells become overactive. The two main consequences of this increased activity are the production of autoantibodies (antibodies that recognize and destroy the body’s own cells) and inflammation that can lead to long-term, irreversible scarring.
The production of autoantibodies in people with lupus and other autoimmune diseases causes the immune system to target the body’s own cells for destruction. For example, about 98% of people with lupus possess antinuclear antibodies (ANA), which can attack the nucleic material of your cells. In addition, some individuals may possess anti-phospholipid antibodies, which damage proteins bound to phospholipids in the membranes of your cells. These autoantibodies are linked to pregnancy complications, stroke, heart attacks, and other blood clots.
In addition, regulatory T cells, which are supposed to control the system, are deficient in SLE.
My white blood cell count is on the low side of normal. How do I activate regulatory T cell (Tregs) action to suppress the anti SS-B antibody?
Concerning Foxp3+ Tregs in SS, several reports suggested that the numbers of Foxp3+ Tregs are positively correlated with SS (11, 12). Sarigui et al. (11) reported that Foxp3+ Tregs were enriched in the salivary glands and associated with the Chisholm score in primary SS. Moreover, Christodoulou et al. (12) reported that minor salivary gland-infiltrating Foxp3+ Tregs were positively correlated with the biopsy focus score, and a lower Foxp3+ cell incidence was correlated with adverse predictors for lymphoma development. These reports clearly suggested that the Foxp3+ Tregs frequency in the salivary glands of SS patients correlate with the prognosis of SS, and even suggested that Foxp3+ Tregs might be associated with pathogenesis of SS.
A number of mechanisms contribute to the capacity of the immune system to discriminate self from non-self, facilitating the maintenance of immunological tolerance to self-antigens and the induction of protective immunity to foreign antigens. Although the removal of immature self-reactive lymphocytes by negative selection in the thymus is considered pivotal to the former process, it is becoming increasingly clear that regulatory T cells (Tregs) are equally important in inducing and maintaining peripheral self-tolerance and thus preventing immune pathologies.
Ah, might want to be careful with increasing Foxp3 suppressor … Too little FoxP3 may lead to autoimmunity, but too much is involved with cancer:
Until recently, Foxp3 expression has been thought to be restricted to the T-cell lineage. However, several lines of evidence indicate that Foxp3 is also expressed by tumor cells. It has been used recently as a biomarker and a prognostic factor for malignant human tumors. A direct link between the presence of Tregs and progression of ovarian carcinoma has been demonstrated where human tumor Foxp3+ Tregs were found to suppress tumor specific immunity and contribute to reduced survival of these patients. In breast cancer, an increase in the Treg population both in peripheral blood and tumor tissues was also reported and a recent study demonstrated a significant intratumoral infiltration of Foxp3+ Tregs in high-risk breast cancer patients and those at risk of late relapse. Given the central contribution of Foxp3 to Treg function, the expression of Foxp3 by tumor cells may represent a novel mechanism by which cancers suppress the immune system to escape destruction.
Now the human breast milk cure for cancer starts to make sense.
Hopefully, drinking raw cows milk from an animal with a properly balanced immune system will help my system adjust. Are Tregs in raw milk destroyed by stomach acid?