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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
B cells are a fundamental component of the body’s immune system. However, like most cells in the body, B cells can become cancerous leading to such diseases as non-Hodgkin’s lymphoma (NHL) and Chronic Lymphocytic Leukemia (CLL). Targeting B-cell surface antigens that are highly expressed in B-cell malignancies with monoclonal antibodies is an ideal treatment strategy as both the B cells and antibodies can come into immediate contact in the bloodstream, and the antibodies can be designed to be highly specific for the individual surface antigens. Antibodies have been developed for several surface antigens including the “cluster of differentiation” or “CD” glycoproteins, found primarily on the surface of B cells (Figure 7.10). Examples include CD20 (targeted by ofatumumab and rituximab) and CD52 (targeted by alemtuzumab). B-lymphocyte surface antigens have also been targeted by Antibody-Drug Conjugates (ADCs) such as ibritumomab tiuxetan and tositumomab (i.e., CD20), brentuximab vedotin (i.e., CD30), and gemtuzumab ozogamicin (i.e., CD33) (see Section 7.3). As discussed above, interaction of the naked antibodies described in this section with their corresponding antigens can lead to cell death through both the ADCC and CDC effects, and also a direct apoptotic effect.
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.
T-cell acute lymphoblastic leukemia: promising experimental drugs in clinical development
Published in Expert Opinion on Investigational Drugs, 2023
Four T-ALL differentiation stages have been historically identified based on the expression of cluster of differentiation (CD) markers (Table 1). Over the last decades, genetic drivers have been identified [21]. The genetic background of T-ALL is widely heterogeneous [21]. Two types of abnormalities have been distinguished [14]. The first type includes abnormalities that cause up-regulation of genes coding for transcription factors critical in T-cell development, maturation, and differentiation: TAL/LMO, HOXA, TLX3, TLX1, NKX2-1/2-2, MEF2C. Their distributions vary between children and adults, but they allow a classification of more than 70% of T-ALL [5]. The second group of abnormalities involves genes that code for various protein families (factors of signaling pathways, tyrosine kinases, ribosomal proteins, epigenetic factors), and is distributed across all genetic subgroups.
Combining locoregional CAR-T cells, autologous + allogeneic tumor lysate vaccination and levamisole in treatment of glioblastoma
Published in Immunopharmacology and Immunotoxicology, 2022
Meric A. Altinoz, Alp Ozpinar, Emily Hacker, Aysel Ozpinar
Intra-CSF application of CAR T-cells does not always guarantee efficient entrance into the brain parenchyma, where glial tumor cells invade. The post-infusion persistence of T lymphocytes must be clarified as preclinical investigations thus far declare varied outcomes. One plausible approach would be intratumoral/locoregional treatment with CAR-T cells. Preclinical studies performed on malignancies strongly support the efficacy of intratumoral CAR-T cell therapy. Globerson-Levin et al. tested (4D5-CD28-γ) CAR-T cells specific to erbB-2 for their tumor inhibition potential in a transgenic mice model expressing high levels of a human erbB-2 that develops breast cancer [18]. CD28 (Cluster of Differentiation 28) is expressed on T cells that supply costimulatory signals necessary for T lymphocyte survival and activation. The 4D5 epitope juxtaposes the transmembrane region of erbB-2. Globerson-Levin’s work revealed that several intratumoral applications of 4D5-CD28-γ CAR-T cells were necessary to eradicate spontaneously arising breast tumors [18]. The authors have concluded that a similar treatment can be employed as neo-adjuvant for endoscopically accessible human malignancies. They also stated that repeated systemic applications of CAR-T cells may target minimal residual disease of relapsing tumors at various body sites or cancers that recur sporadically during treatment.