Biological response modifiers

Biological response modifiers (BRMs) are substances that modify immune responses. They can be both endogenous (produced naturally within the body) and exogenous (as pharmaceutical drugs), and they can either enhance an immune response or suppress it. Some of these substances arouse the body's response to an infection, and others can keep the response from becoming excessive. Thus they serve as immunomodulators in immunotherapy (therapy that makes use of immune responses), which can be helpful in treating cancer (where targeted therapy often relies on the immune system being used to attack cancer cells) and in treating autoimmune diseases (in which the immune system attacks the self), such as some kinds of arthritis and dermatitis. Most BRMs are biopharmaceuticals (biologics), including monoclonal antibodies, interleukin 2, interferons, and various types of colony-stimulating factors (e.g., CSF, GM-CSF, G-CSF). "Immunotherapy makes use of BRMs to enhance the activity of the immune system to increase the body's natural defense mechanisms against cancer",[1] whereas BRMs for rheumatoid arthritis aim to reduce inflammation.

Some of the effects of BRMs include nausea and vomiting, diarrhea, loss of appetite, fever and chills, muscle aches, weakness, skin rash, an increased tendency to bleed, or swelling.

Abciximab

Mechanism of action: A monoclonal antibody that binds to the glycoprotein receptor IIb/IIIa on activated platelets, preventing aggregation. Clinical use: Acute coronary syndromes, percutaneous transluminal coronary angioplasty. Toxicity: Bleeding, thrombocytopenia.

Anakinra (Kineret)

Mechanism of action: A recombinant version of the Interleukin 1 receptor antagonist. Clinical use: Rheumatoid arthritis. Toxicity: Allergic response & neutropenia.

Etanercept (Enbrel)

Mechanism of action: Recombinant form of human TNF receptor that binds TNF. Clinical use: Rheumatoid arthritis, psoriasis, ankylosing spondylitis.

Infliximab (Remicade)

Mechanism of action: A monoclonal antibody to TNF, proinflammatory cytokine. Clinical use: Crohn's disease, rheumatoid arthritis, ankylosing spondylitis. Toxicity: Respiratory infection, fever, hypotension. Predisposes to infections (reactivation of latent TB).

Rituximab (Rituxan)

Mechanism of action: A monoclonal antibody to CD20 surface immunoglobulin. Clinical use: Lymphoma and a variety of autoimmune diseases, although it may be ineffective in treating IgA-mediated diseases.[2]

Trastuzumab (Herceptin)

Mechanism of action: A monoclonal antibody against HER2/neu (erb-B2). Helps kill breast cancer cells that overexpress HER-2, possibly through antibody-dependent cytotoxicity. Clinical use: Metastatic breast cancer. Toxicity: Cardiotoxicity.

Natural BRMs

Extracts from some medicinal mushrooms are natural biological response modifiers.[3]

See also

References

  1. ↑ "Biological Response Modifiers (BRM)".
  2. ↑ He Y, Shimoda M, Ono Y, Villalobos IB, Mitra A, Konia T, Grando SA, Zone JJ, Maverakis E (2015). "Persistence of Autoreactive IgA-Secreting B Cells Despite Multiple Immunosuppressive Medications Including Rituximab". JAMA Dermatol. 151 (6): 646–50. doi:10.1001/jamadermatol.2015.59. PMID 25901938.
  3. ↑ Tzianabos AO (2000). "Polysaccharide immunomodulators as therapeutic agents: structural aspects and biologic function.". Clin Microbiol Rev. 13 (4): 523–33. doi:10.1128/CMR.13.4.523-533.2000. PMC 88946Freely accessible. PMID 11023954.
This article is issued from Wikipedia - version of the 10/14/2016. The text is available under the Creative Commons Attribution/Share Alike but additional terms may apply for the media files.