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Specific Host Restance: The Effector Mechanisms
Published in Julius P. Kreier, Infection, Resistance, and Immunity, 2022
All of the effector responses of cell-mediated immunity require activation by T cells1. This means that with the elimination of T cells, the cell-mediated protective response is eliminated. There are two basic classes of T cells that can be distinguished by CD (short for cluster of differentiation) marker proteins on their surface. CD4+ cells include the infiammatory T cells (TH1) and the helper T cells (TH2). CD8+ cells are the cytotoxic T cells. Because of the affinity of the CD4 protein for the human immunodeficiency virus (HIV), it is this class of T cells that is destroyed in peopie with AIDS. The severe immunodeficiency that results is the direct consequence of the destruction of CD4+ cells.
Sexual health
Published in Sally Robinson, Priorities for Health Promotion and Public Health, 2021
Rajeeb Kumar Sah, Sally Robinson
Human immunodeficiency virus (HIV), like most viruses, needs a host cell where it replicates to survive. In humans, the host cell for HIV is part of the immune system which protects the body from infections. HIV invades the ‘cluster of differentiation 4 (CD4)’ cells, also called T helper cells. As it destroys these cells, the normal processes of protection cease and the immune system gradually weakens. The body is increasingly unable to fight against everyday infections and diseases. Individuals become vulnerable to opportunistic infections such as tuberculosis and pneumonia; this develops into a condition known as acquired immunodeficiency syndrome (AIDS).
Antibody-Based Therapies
Published in David E. Thurston, Ilona Pysz, Chemistry and Pharmacology of Anticancer Drugs, 2021
Finally, the targeted antigen has to be carefully chosen to be highly expressed by the tumor cells but with no or limited expression by healthy cells. Leading examples include the “Cluster of Differentiation” or “CD” glycoproteins found primarily on the surface of B cells (e.g., CD19, CD20, CD30, CD33, and CD52), which have been successfully used to develop both mAbs (e.g., CD20: Rituximab, RituxanTM or MabTheraTM) and ADCs (e.g., CD30: Brentuximab vedotin, AdcetrisTM) to treat various types of leukemia. Similarly, Her2, which is found on the surface of some breast tumor cells, has been successfully exploited to develop both MAbs (e.g., trastuzumab, HerceptinTM) and ADCs (e.g., ado-trastuzumab emtansine, KadcylaTM).
Maintaining a ‘fit’ immune system: the role of vaccines
Published in Expert Review of Vaccines, 2023
Béatrice Laupèze, T. Mark Doherty
The kind of innate immune response that develops in the earliest stages of immune recognition can help shape the nature of the adaptive immune response that subsequently develops; for example, by altering the proportion of B cells that differentiate into plasma cells releasing into the bloodstream antigen-specific antibodies (immunoglobulin G [IgG]), and the proportion of those that migrate to mucosal surfaces such as the respiratory system or the gut and release IgA [16]. This differential response leads to the development of the different populations of memory cells that are capable of responding rapidly and appropriately to subsequent exposures to that specific pathogen. Likewise, the type of T cells that develop after activation by APCs influences the inflammatory mediators released by the activated cluster of differentiation 4 positive (CD4+) T helper (Th) cell sub-populations (Th1, Th2, Th17, Tfh), which in turn influence how effectively the pathogen can be removed or contained [17]. CD8+ cytotoxic T cells activated by the innate response can also activate a range of different behaviors, such as killing cells directly or via the release of cytotoxins.
Clinical efficacy and safety of bispecific antibodies for the treatment of solid tumors: a systematic review and meta-analysis
Published in Expert Review of Anticancer Therapy, 2023
Seyed Aria Nejadghaderi, Maryam Balibegloo, Maryam Noori, Farimah Fayyaz, Amene Saghazadeh, Nima Rezaei
A large number of BsAbs are developed or are currently being evaluated in trials. So far, the United States Food and Drug Administration has approved four BsAbs. Blinatumomab, which targets cluster of differentiation (CD)3 and CD19 and is used to treat relapsed/refractory precursor B-cell acute lymphoblastic leukemia (ALL), was approved in 2014 [6,7]. Emicizumab was approved in 2017 to treat hemophilia A through binding to factors IXa and X [8,9]. On 21 May 2021, amivantamab, a BsAb targeting epidermal growth factor receptor (EGFR) and mesenchymal-epithelial transition factor (MET), received its approval [10]. Lastly, Tebentafusp was approved as a BsAb that targets gp100 peptide-HLA-A*02:01 and CD3 to treat HLA-A*02:01-positive adults with unresectable or metastatic uveal melanoma in January 2022 [11]. Catumaxomab, approved by European Union in 2009, targets epithelial cell adhesion molecule (EpCAM) and CD3 and treats malignant ascites in patients with EpCAM-positive malignant solid tumors [12,13]. However, its approval was withdrawn due to commercial reasons in 2017.
Novel corona virus (COVID-19) pandemic: current status and possible strategies for detection and treatment of the disease
Published in Expert Review of Anti-infective Therapy, 2022
Stuti Bhagat, Nisha Yadav, Juhi Shah, Harsh Dave, Shachee Swaraj, Shashank Tripathi, Sanjay Singh
An effective vaccine is necessary to prevent, eradicate, and avoid recurrence of the outbreak of COVID-19. So far, no vaccine for COVID-19 has been developed; however, several worldwide studies are in different clinical trials. Various strategies are being pursued, including considering the development of recombinant protein (such as S protein) from similar viruses such as SARS-CoV and MERS-CoV [193]. During the outbreaks of SARS and MERS, various vaccination strategies were developed to control the infection and tested in vivo models, but none was studied in clinical trials. The vaccination strategies include inactivated viral vaccine, live-attenuated viral vaccine, viral vector vaccine, subunit (S protein) vaccine, and DNA vaccine [194] (Figure 5(a)). During the exposure of vaccines or viral antigens to the human body, the viral load is processed in two ways (Figure 5(b)). 1) Antigen-presenting cells (APCs), like macrophage and dendritic cells, engulf the viral antigen and present it to TH cells via major histocompatibility complex (MHC) II molecules. Further, the TH cells activate the cluster of differentiation 8 (CD8) +ve killer T cells (Cytotoxic T cells- CTLs). 2) The infected cells can also activate CTLs via the interaction with MHC I molecules. These activated CTLs proliferate and differentiate into effector CTLs (which eventually kills the infected cells with the virus) and memory CTLs. On the other side, TH cells activate and prime the B cells, which proliferate and differentiate into antibody-producing plasma cells and memory cells [195].