Chronic inflammation is also referred to as slow, long-term inflammation lasting for prolonged periods of several months to years. Generally, the extent and effects of chronic inflammation vary with the cause of the injury and the ability of the body to repair and overcome the damage.
The main phagocytes involved in acute inflammation are the neutrophils, a type of white blood cell that contains granules of cell-destroying enzymes and proteins. When tissue damage is slight, an adequate supply of these cells can be obtained from those already circulating in the blood.
Although innate immune stimuli may contribute to chronic inflammation, the adaptive immune system may also be involved because T lymphocyte-producing cytokines are powerful inducers of inflammation.
When you're living with chronic inflammation, your body's inflammatory response can eventually start damaging healthy cells, tissues, and organs. Over time, this can lead to DNA damage, tissue death, and internal scarring. All of these are linked to the development of several diseases, including: cancer.
The initial inflammatory response is usually acute, and may or may not evolve into chronic inflammation. However, chronic inflammation is not always preceded by an acute phase. Although usually beneficial to the organism, inflammation itself may lead to tissue damage, resulting in escalation of chronic inflammation.
These strategies might include:
- eating a diet rich in fruits and vegetables.
- exercising regularly.
- maintaining a healthy weight.
- quitting smoking.
- drinking alcohol only in moderation.
- getting enough sleep.
- avoiding infection through regular hand washing.
- reducing stress.
The role of B cells in autoimmune diseases involves different cellular functions, including the well-established secretion of autoantibodies, autoantigen presentation and ensuing reciprocal interactions with T cells, secretion of inflammatory cytokines, and the generation of ectopic germinal centers.
Without B-cells, your body would not be as effective at fighting off a number of common bacteria and viruses; and you would lack the long-lasting "memory antibody" function that is typical after recovering from an infection or after being immunized against a specific infectious invader.
Targeting B cell subsetsChan et al's2 and others studies suggest that depletion of autoantigen presenting B cells may reduce autoimmune disease progression. Furthermore, B cell APCs in inflamed synovium or cytokine producing B cells near or in the synovium may also be targets of CD20 based therapy.
Orally bioavailable inhibitors of spleen tyrosine kinase, Bruton's tyrosine kinase, or PI3Kδ, induce high rates of durable responses. Ibrutinib, a covalent inhibitor of Bruton's tyrosine kinase, and idelalisib, a selective inhibitor of PI3Kδ, have obtained regulatory approval in chronic lymphocytic leukemia.
Table 1
| Agent | Type of Therapy | B-cell Lineages Affected |
|---|
| Rituximab | Anti-CD20 | From pre-B cells to memory cells |
| Ocrelizumab | Anti-CD20 | From pre-B cells to memory cells |
| Ofatumumab | Anti-CD20 | From pre-B cells to memory cells |
| Epratuzumab | Anti-CD22 | Mature CD27 cells |
A primary feature of autoimmune diseases is the loss of B-cell tolerance and the inappropriate production of autoantibodies. More than 80 distinct autoimmune diseases have been described, such as multiple sclerosis (MS), rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE).
B-cell lymphoma refers to a group of cancers that attack the immune system. It is the most common type of non-Hodgkin lymphoma. The cancer grows in the B cells, also called B lymphocytes, which make antibodies to attack invading pathogens. B-cell lymphoma is a type of non-Hodgkin lymphoma.
Rituximab depletion of B cells leads to a sharp and sustained rise in BAFF levels, and it is this anti-apoptotic cytokine that acts to restore B-cell numbers by increasing the survival rate of immature B cells [23,44].
B cells are activated when their B cell receptor (BCR) binds to either soluble or membrane bound antigen. In their inactivated state B cells express IgM/IgD but once activated they may express IgA, IgE, IgG or retain IgM expression. They do this by excision of the unwanted isotypes (Figure 1).
Types of B Lymphocytes
- Plasma Cell. Once activated, B lymphocytes can differentiate into plasma cells.
- Memory B Lymphocyte. Some B lymphocytes will differentiate into memory B cells, which are are long-lived cells that remain within the body and allow a more rapid response to future infections.
- T-independent B Lymphocyte.
B cells are a type of lymphocyte that are responsible for the humoral immunity component of the adaptive immune system. These white blood cells produce antibodies, which play a key part in immunity. Each B cell contains a single round nucleus.
An increased B cell count may be due to: Chronic lymphocytic leukemia. DiGeorge syndrome. Multiple myeloma.
In addition to the spleen and lymph nodes, memory B cells are found in the bone marrow, Peyers' patches, gingiva, mucosal epithelium of tonsils, the lamina propria of the gastro-intestinal tract, and in the circulation (67, 71–76). Initially, during B cell development in the bone marrow, the antibody molecules are inserted into the plasma membrane, where they serve as receptors for antigen. The effector cells secrete antibodies with the same unique antigen-binding site as the membrane-bound antibodies.
