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An Introduction to the Immune System and Vaccines
Published in Patricia G. Melloy, Viruses and Society, 2023
One could say that the innate branch reacts the same way to all viruses. An everyday example is if you were a boxer and lashed out with all your might against a new opponent in the boxing ring in a way dependent on your existing skills and your reach, not specific to the opponent (Figure 2.1). During the innate response, cells release signaling molecules such as cytokines like interferon (IFN) Type I and II that tell cells to prepare for a fight (Lostroh 2019). Cytokines have been described as “biological response modifiers” (Cruse and Lewis 2009). Also, special white blood cells called neutrophils can move into an area of the tissue to engulf foreign invaders through phagocytosis “cell eating” (Lostroh 2019). Typical side effects of this early response are fever and inflammation.
Treatment of Chronic Fatigue Syndrome
Published in Jay A. Goldstein, Chronic Fatigue Syndromes, 2020
Kutapressin is a porcine liver extract of low molecular weight peptides which are thought to have an immunomodulatory action, since results on a test of mitogen stimulation, the single lymphocyte immune function, improve if initially suppressed. Kutapressin is given by intramuscular injection. Results have been excellent as reported in open trials by experimenters from Houston.25 Many of us do not find the response to be nearly that good, and some CFS clinicians have stopped using it altogether. Active peptides from the parent Kutapressin have been isolated. This presumably more potent biological response modifier will be starting clinical trials shortly.
Biological Response Modifiers and Chemotherapeutic Agents that Alter Interleukin 2 Activities
Published in Ronald H. Goldfarb, Theresa L. Whiteside, Tumor Immunology and Cancer Therapy, 2020
William L. West, Allen R. Rhoads, Clement O. Akogyeram
Immunopharmacology has as its goal the identification of agents that act on specific components of the immune system to either selectively enhance or suppress their activities. In a cancer-bearing host, agents of interest that modulate the immune system are of two general types: (a) immunosuppressants which are used as cytotoxic agents in cancer therapy and (b) biological response modifiers (BRMs) which enhance the immune response. More generally, BRMs are defined as those agents which modify a biological response to tumor cells with resultant therapeutic benefits. BRMs, whether biologic or chemical agents, are capable of restoring an immunologic balance in tumor-bearing hosts by enhancing antitumor functions of the immune system. In this respect, BRMs differ from classical modalities (surgery, radiation, and chemotherapy) used in therapy of cancer. Although most BRMs are investigational drugs, they present approaches that expand the possibility for successful treatment of conditions associated with altered immunological functions including cancer.
Targeted therapies for autoimmune/idiopathic nonmalignant diseases: risk and management of opportunistic infections
Published in Expert Opinion on Drug Safety, 2020
Davide Fiore Bavaro, Deborah Fiordelisi, Gioacchino Angarano, Laura Monno, Annalisa Saracino
The management of patients affected by many autoimmune/idiopathic diseases [1], malignancies, and organ transplants [2] has been revolutionized by the development of the so-called ‘biological drugs,’ usually named ‘Biologics,’ the first of which dates back to 1986 [3]. This term indicates a wide family of products, which are directed against many different targets; consequently, they can be classified on the basis of their mode of action, targeted site, or structural properties. [4] However, from a clinical point of view, at least three main categories can be distinguished: i. biological response modifiers (‘BRMs’: agents that exert a stimulating effect either enhancing or suppressing the immune system, e.g. interferons, interleukins, colony stimulating factors, etc.), ii. gene therapies (which act by replacing defective genes, stimulating immune response, changing drug activation state, blocking antiapoptotic mechanisms, using altered viruses to kill cancer cells, etc.), iii. targeted therapies (‘TT’: directly targeting the cells or pathways involved in disease pathophysiology, thus sparing normal tissues) [5]. TT can also be divided into monoclonal antibodies (mAb) and small molecules enzyme inhibitors. Notably, because of their remarkable efficacy in inhibiting the inflammatory cascade and slowing down the progression of autoimmune diseases, these molecules are considered essential in many clinical settings, and, in fact, numerous products are currently available and approved in various medical specialties [6].
Tocilizumab Employment in the Treatment of Resistant Juvenile Idiopathic Arthritis Associated Uveitis
Published in Ocular Immunology and Inflammation, 2021
Arash Maleki, Ambika Manhapra, Soheila Asgari, Peter Y. Chang, C. Stephen Foster, Stephen D. Anesi
There were limitations of our study, since it was a retrospective study with a small sample size. In addition, we did not have a control group for comparison. This can be justified by the fact that all of patients in the study were resistant to at least one conventional IMT and biological response modifier agent. Continuing former conventional IMT might be another drawback of our study, since the effectiveness of IV-TCZ could be related to the synergistic effect of IV-TCZ in combination with other IMTs, and not the IV-TCZ itself.
The expression of IL-1β can deteriorate the prognosis of nervous system after spinal cord injury
Published in International Journal of Neuroscience, 2018
Tao Li, Yu-tang Li, Di-yu Song
Spinal cord injury is often caused by different degrees of injury which could cause different degrees of motor sensory dysfunction and had serious effect on the quality of life. Although the related diagnosis and treatment technology continue to improve in recent years, the prognosis of patients is still not very ideal and this research had always been a hot spot [1]. Secondary damage plays an important role in spinal cord injury, which is mainly due to the inflammation after trauma. Anakinra and other drugs are used to block or weaken associated inflammatory response regulator to relieve the reperfusion injury after spinal cord injury in the new treatment strategies. Primary spinal damage could lead to the irreversible death of neurons and continue to be lost within a few hours. There are some biochemistry and cellular and molecular mechanism involved in the progress of secondary neuronal death, and the main inflammatory reaction occurs mainly in the local spinal cord injury [2–5]. Present studies show that microglia is the main source of tumor necrosis factor α (TNF-α) and interleukin-1β (IL-1β), which could reduce the number of oligodendrocytes [6]. It is reported that the synthesis and secretion of IL-1β at injury site had increased in 1 h after spinal cord injury. IL-1β was involved in cell proliferation, differentiation, apoptosis and other cellular activity as an important mediator of the inflammatory reaction [7]. Anakinra could block the inflammatory reaction and slowed the degradation of cartilage as IL-1 receptor antagonist in the treatment of rheumatoid arthritis. So it is considered as a ‘biological response modifier’, which could target select pathological factors in the treatment [4,8–10]. Based on this study, we used a rat model of spinal cord injury and used Anakinra to intervene at the same time to assess changes in cases of histologically and related biochemical indexes, to explore the effect of drug intervention, to provide guidance and reference value for clinical diagnosis and treatment and basic research.