Target type: biologicalprocess
Any process leading to negative selection in B cells. Mechanisms of negative selection include anergy and deletion. [GOC:jal]
B cell negative selection is a critical process in the development of a healthy immune system. It eliminates autoreactive B cells, those that recognize and bind to self-antigens, preventing autoimmune diseases. This process occurs in the bone marrow, the primary site of B cell development.
During B cell maturation, immature B cells undergo a series of rearrangements of their immunoglobulin genes, creating a vast repertoire of antigen receptors. These receptors are displayed on the surface of the B cells, allowing them to interact with antigens.
Negative selection occurs when an immature B cell encounters a self-antigen in the bone marrow. This interaction can trigger several outcomes:
1. **Apoptosis (programmed cell death):** If the interaction is strong and persistent, the B cell will undergo apoptosis and be eliminated.
2. **Receptor editing:** In some cases, the B cell can attempt to "edit" its receptor by rearranging its immunoglobulin genes again. This may result in a new receptor that no longer recognizes the self-antigen.
3. **Anergy:** If receptor editing fails or is not possible, the B cell may become anergic. Anergy is a state of unresponsiveness, where the B cell can no longer be activated by its specific antigen.
These mechanisms ensure that only B cells with receptors that recognize foreign antigens are allowed to mature and enter the circulation. This rigorous selection process is essential for maintaining self-tolerance and preventing autoimmune diseases.
The removal of autoreactive B cells is a dynamic process that relies on the presentation of self-antigens by specialized cells in the bone marrow. These cells include stromal cells, macrophages, and dendritic cells. They express a diverse range of self-antigens that B cells are exposed to during their development.
Negative selection is a complex and tightly regulated process. It involves a variety of signaling pathways and molecules that control the fate of B cells. Defects in these pathways can lead to autoimmune diseases.
The successful elimination of autoreactive B cells through negative selection is a fundamental aspect of a healthy immune system. This process plays a vital role in preventing the development of autoimmune diseases by ensuring that the immune system does not attack the body's own tissues.'
"
Protein | Definition | Taxonomy |
---|---|---|
Bcl-2 homologous antagonist/killer | A Bcl-2 homologous antagonist/killer that is encoded in the genome of human. [PRO:WCB, UniProtKB:Q16611] | Homo sapiens (human) |
Apoptosis regulator BAX | An apoptosis regulator BAX that is encoded in the genome of human. [PRO:SY, UniProtKB:Q07812] | Homo sapiens (human) |
Compound | Definition | Classes | Roles |
---|---|---|---|
vorinostat | vorinostat : A dicarboxylic acid diamide comprising suberic (octanedioic) acid coupled to aniline and hydroxylamine. A histone deacetylase inhibitor, it is marketed under the name Zolinza for the treatment of cutaneous T cell lymphoma (CTCL). Vorinostat: A hydroxamic acid and anilide derivative that acts as a HISTONE DEACETYLASE inhibitor. It is used in the treatment of CUTANEOUS T-CELL LYMPHOMA and SEZARY SYNDROME. | dicarboxylic acid diamide; hydroxamic acid | antineoplastic agent; apoptosis inducer; EC 3.5.1.98 (histone deacetylase) inhibitor |
alexidine dihydrchloride | |||
6-n-tridecylsalicylic acid | 6-n-tridecylsalicylic acid: structure given in first source | hydroxybenzoic acid | |
5,6-dehydrokawain | 5,6-dehydrokawain: from Alpinia speciosa rhizoma; RN given for cpd without isomeric designation; structure given in first source | 2-pyranones; aromatic ether | |
abt-737 | aromatic amine; aryl sulfide; biphenyls; C-nitro compound; monochlorobenzenes; N-arylpiperazine; N-sulfonylcarboxamide; secondary amino compound; tertiary amino compound | anti-allergic agent; anti-inflammatory agent; antineoplastic agent; apoptosis inducer; B-cell lymphoma 2 inhibitor | |
meiogynin a | meiogynin A: from the bark of Meiogyne cylindrocarpa; structure in first source | ||
jy-1-106 | JY-1-106: a BH3 alpha-helix mimetic that functions as a pan-Bcl-2 inhibitor; structure in first source |