which of the following is true about cd4+ t lymphocytes course hero

CD4 + T lymphocytes, as previously discussed, are responsible for the majority of HIV replication in the periphery. HIV-1 may enter the CNS in infected lymphocytes, although this is more frequent in late stage disease. Activated T-cells enter the CNS.

Full Answer

What are CD4 and T lymphocytes?

What is the role of T lymphocytes in adaptive immune responses?

What are the targets of HIV-1?

What is the role of IL-5 in the development of eosinophils?

What are the cytokines in asthma?

What is the role of T helper cells in the development of antibody?

Which lymphocytes help B lymphocytes switch to the synthesis and secretion of IgE antibodies?

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What are CD4 and T lymphocytes?

CD4 + T lymphocyte subsets are categorized on the basis of their cellular functions and capacity to secrete specific cytokines. CD4 + Th2 lymphocytes evolved to mediate type 2 immune responses to helminths and parasites, but they are also central to mechanisms of atopy and asthma. IL-4 is the most potent Th2 polarizing factor, 164 and Th2 cells secrete IL-4, IL-5, IL-9, and IL-13. 127-129 There is evidence in human asthma for an excess of CD4 + Th2 lymphocytes in the airway. Lavage fluid from asthmatic subjects has increased numbers of T cells expressing mRNA for IL-4 and IL-5 (but not IFN-γ). 165 Subsequent studies have confirmed either an excess of Th2 lymphocytes or increases in Th2 cytokine transcripts, protein, or activity in the airway. 166,167 CD4 + Th2 cells are not the sole source of Th2 cytokines because mast cells, basophils, and ILC2 cells also secrete these cytokines, but they do appear to be the dominant source in chronic established disease. CD4 + Th2 cells are CCR4 + and are responsive to CCL17 (also called thymus and activation-regulated chemokine, TARC), which is an epithelial cell-derived chemokine important for Th2 cell accumulation in the airway (see Fig. 41-5 ). CD4 + Th2 cells also display multiple other receptors, including CRTH2, ST2, TSLPR, and IL17BR, which means that they can also respond to PGD2, IL-33, TSLP, and IL-25, respectively. 168 IL-5 from Th2 cells promotes tissue eosinophilia, whereas IL-9 promotes mast cell hyperplasia, and IL-13 causes epithelial cell activation, as described earlier.

What is the role of T lymphocytes in adaptive immune responses?

This suggests that T-lymphocyte-mediated help is most likely a late evolutionary addition to adaptive immune responses. Activation of B lymphocytes in the presence of T lymphocytes alters the isotype of antibody produced, thus increasing the number of protective mechanisms (complement activation and ADCC by IgG, survival of IgA in the gastrointestinal and respiratory tracts, degranulation of mast cells by IgE) that can be recruited in response to potential pathogens. In addition, B lymphocytes assisted by T lymphocytes develop into memory cells that respond rapidly and with greater vigor upon subsequent challenge with the sensitizing antigen.

What are the targets of HIV-1?

Activated CD4 + T lymphocytes represent the main cellular target of HIV-1, and most of these cells reside in the gastrointestinal tract. During acute infection, adolescents and adults frequently have nonspecific “viral” symptoms (see Chapter 111 ), but infants usually are symptom free. 1,2 In adolescents and adults, plasma viremia decreases and peripheral blood CD4 + T-lymphocyte counts rise after a few weeks, even in the absence of ART. CD8 + cytotoxic T lymphocytes (CTLs) play a major role in this early control of viral replication. 3–5 Additional adaptive immune responses, as well as innate immune responses, increasingly are being recognized as important factors in the control of initial viral replication. 6–8 After this acute period, adults and older children have relatively constant levels of viremia, which is referred to as a set point. This level of viremia is highly predictive of the later course of disease progression. 9,10

What is the role of IL-5 in the development of eosinophils?

IL-5, together with IL-3 and granulocyte-macrophage colony-stimulating factor (GM-CSF), promotes the differentiation and maturation of eosinophil progenitors (CD34 + cells) in the bone marrow and induces the release of mature eosinophils from the bone marrow into the circulation. Although IL-3 and GM-CSF also promote the differentiation of multiple cell lineages, IL-5 promotes only the terminal differentiation of eosinophils. IL-5 has also been shown to be important for the survival of eosinophils once in the tissues and for priming eosinophils for response to several stimuli. Clinically, the presence of eosinophils in the airways (and in the circulation) is associated with the presence of asthma, suggesting that eosinophil-induced damage to the pulmonary epithelium causes BHR and asthma. However, studies have shown that the depletion of eosinophils in patients with asthma through neutralization of IL-5 with anti-IL-5 monoclonal antibody does not reduce BHR, 9 except in a small fraction of patients, who have very large numbers of airway eosinophils. 10,11 Eosinophils produce cysteinyl leukotrienes, and may enhance the production of IL-13 12 which can directly induce BHR (see below).

What are the cytokines in asthma?

CD4 + T lymphocytes producing Th2 cytokines play a prominent role in asthma and are present in lung biopsy specimens and bronchoalveolar lavage (BAL) fluid from patients with asthma. 5 Several studies showed a correlation between the presence of CD4 + Th2 cells and Th2 cytokine levels with the severity of asthma. 6 Although several cell types produce Th2 cytokines, including mast cells, basophils and natural killer T (NKT) cells, Th2 lymphocytes are considered fundamental in asthma, because in animal models, CD4 + T cell depletion prevents the development of asthma. In fact, B cell-, IgE-, and mast cell-deficient mice can still develop asthma, whereas CD4 -, STAT-6-, and interleukin (IL)-13-deficient mice cannot. The signature Th2 cytokine, IL-4, plays an important initiator role. IL-4 is essential for the differentiation of Th2 lymphocytes, and in the absence of IL-4, Th2 cell differentiation is severely impaired. IL-4 is critical for the induction of IgE synthesis and for the up-regulation of IgE receptor expression on B cells (low affinity IgE receptor, CD23), mast cells, and basophils (high affinity IgE receptor, FcεRI). Inhalation of recombinant IL-4 leads to BHR and eosinophil recruitment in asthmatic people. 7 IL-4 also increases the production of cysteinyl leukotrienes from IgE-primed mast cells 8 and induces expression of adhesion molecules, such as vascular cell adhesion molecule-1 (VCAM-1) on pulmonary endothelium, which is involved in the recruitment of eosinophils, basophils, and lymphocytes. IL-4 induces expression of eotaxin by lung cells, although IL-13, another Th2 cytokine, is more potent in this regard. In addition, IL-4 increases mucus production and may have direct effects on smooth muscle cells, but the exact role of IL-4 in causing BHR and mucus production is complex and overlaps with that of IL-13 (see below).

What is the role of T helper cells in the development of antibody?

These investigators demonstrated that while thymus-derived (T) lymphocytes do not themselves produce antibody, they are essential to help bone marrow-derived (B) lymphocytes synthesize optimal amounts of antibody. The mechanism of collaboration between T helper and B lymphocytes involves both cell-to-cell contact and the release of cytokines. Details of the experimental design used by these three groups are presented in Chapter 13.

Which lymphocytes help B lymphocytes switch to the synthesis and secretion of IgE antibodies?

T H 2 lymphocytes that help B lymphocytes switch to the synthesis and secretion of IgE antibodies.

What are CD4 and T lymphocytes?

CD4 + T lymphocyte subsets are categorized on the basis of their cellular functions and capacity to secrete specific cytokines. CD4 + Th2 lymphocytes evolved to mediate type 2 immune responses to helminths and parasites, but they are also central to mechanisms of atopy and asthma. IL-4 is the most potent Th2 polarizing factor, 164 and Th2 cells secrete IL-4, IL-5, IL-9, and IL-13. 127-129 There is evidence in human asthma for an excess of CD4 + Th2 lymphocytes in the airway. Lavage fluid from asthmatic subjects has increased numbers of T cells expressing mRNA for IL-4 and IL-5 (but not IFN-γ). 165 Subsequent studies have confirmed either an excess of Th2 lymphocytes or increases in Th2 cytokine transcripts, protein, or activity in the airway. 166,167 CD4 + Th2 cells are not the sole source of Th2 cytokines because mast cells, basophils, and ILC2 cells also secrete these cytokines, but they do appear to be the dominant source in chronic established disease. CD4 + Th2 cells are CCR4 + and are responsive to CCL17 (also called thymus and activation-regulated chemokine, TARC), which is an epithelial cell-derived chemokine important for Th2 cell accumulation in the airway (see Fig. 41-5 ). CD4 + Th2 cells also display multiple other receptors, including CRTH2, ST2, TSLPR, and IL17BR, which means that they can also respond to PGD2, IL-33, TSLP, and IL-25, respectively. 168 IL-5 from Th2 cells promotes tissue eosinophilia, whereas IL-9 promotes mast cell hyperplasia, and IL-13 causes epithelial cell activation, as described earlier.

What is the role of T lymphocytes in adaptive immune responses?

This suggests that T-lymphocyte-mediated help is most likely a late evolutionary addition to adaptive immune responses. Activation of B lymphocytes in the presence of T lymphocytes alters the isotype of antibody produced, thus increasing the number of protective mechanisms (complement activation and ADCC by IgG, survival of IgA in the gastrointestinal and respiratory tracts, degranulation of mast cells by IgE) that can be recruited in response to potential pathogens. In addition, B lymphocytes assisted by T lymphocytes develop into memory cells that respond rapidly and with greater vigor upon subsequent challenge with the sensitizing antigen.

What are the targets of HIV-1?

Activated CD4 + T lymphocytes represent the main cellular target of HIV-1, and most of these cells reside in the gastrointestinal tract. During acute infection, adolescents and adults frequently have nonspecific “viral” symptoms (see Chapter 111 ), but infants usually are symptom free. 1,2 In adolescents and adults, plasma viremia decreases and peripheral blood CD4 + T-lymphocyte counts rise after a few weeks, even in the absence of ART. CD8 + cytotoxic T lymphocytes (CTLs) play a major role in this early control of viral replication. 3–5 Additional adaptive immune responses, as well as innate immune responses, increasingly are being recognized as important factors in the control of initial viral replication. 6–8 After this acute period, adults and older children have relatively constant levels of viremia, which is referred to as a set point. This level of viremia is highly predictive of the later course of disease progression. 9,10

What is the role of IL-5 in the development of eosinophils?

IL-5, together with IL-3 and granulocyte-macrophage colony-stimulating factor (GM-CSF), promotes the differentiation and maturation of eosinophil progenitors (CD34 + cells) in the bone marrow and induces the release of mature eosinophils from the bone marrow into the circulation. Although IL-3 and GM-CSF also promote the differentiation of multiple cell lineages, IL-5 promotes only the terminal differentiation of eosinophils. IL-5 has also been shown to be important for the survival of eosinophils once in the tissues and for priming eosinophils for response to several stimuli. Clinically, the presence of eosinophils in the airways (and in the circulation) is associated with the presence of asthma, suggesting that eosinophil-induced damage to the pulmonary epithelium causes BHR and asthma. However, studies have shown that the depletion of eosinophils in patients with asthma through neutralization of IL-5 with anti-IL-5 monoclonal antibody does not reduce BHR, 9 except in a small fraction of patients, who have very large numbers of airway eosinophils. 10,11 Eosinophils produce cysteinyl leukotrienes, and may enhance the production of IL-13 12 which can directly induce BHR (see below).

What are the cytokines in asthma?

CD4 + T lymphocytes producing Th2 cytokines play a prominent role in asthma and are present in lung biopsy specimens and bronchoalveolar lavage (BAL) fluid from patients with asthma. 5 Several studies showed a correlation between the presence of CD4 + Th2 cells and Th2 cytokine levels with the severity of asthma. 6 Although several cell types produce Th2 cytokines, including mast cells, basophils and natural killer T (NKT) cells, Th2 lymphocytes are considered fundamental in asthma, because in animal models, CD4 + T cell depletion prevents the development of asthma. In fact, B cell-, IgE-, and mast cell-deficient mice can still develop asthma, whereas CD4 -, STAT-6-, and interleukin (IL)-13-deficient mice cannot. The signature Th2 cytokine, IL-4, plays an important initiator role. IL-4 is essential for the differentiation of Th2 lymphocytes, and in the absence of IL-4, Th2 cell differentiation is severely impaired. IL-4 is critical for the induction of IgE synthesis and for the up-regulation of IgE receptor expression on B cells (low affinity IgE receptor, CD23), mast cells, and basophils (high affinity IgE receptor, FcεRI). Inhalation of recombinant IL-4 leads to BHR and eosinophil recruitment in asthmatic people. 7 IL-4 also increases the production of cysteinyl leukotrienes from IgE-primed mast cells 8 and induces expression of adhesion molecules, such as vascular cell adhesion molecule-1 (VCAM-1) on pulmonary endothelium, which is involved in the recruitment of eosinophils, basophils, and lymphocytes. IL-4 induces expression of eotaxin by lung cells, although IL-13, another Th2 cytokine, is more potent in this regard. In addition, IL-4 increases mucus production and may have direct effects on smooth muscle cells, but the exact role of IL-4 in causing BHR and mucus production is complex and overlaps with that of IL-13 (see below).

What is the role of T helper cells in the development of antibody?

These investigators demonstrated that while thymus-derived (T) lymphocytes do not themselves produce antibody, they are essential to help bone marrow-derived (B) lymphocytes synthesize optimal amounts of antibody. The mechanism of collaboration between T helper and B lymphocytes involves both cell-to-cell contact and the release of cytokines. Details of the experimental design used by these three groups are presented in Chapter 13.

Which lymphocytes help B lymphocytes switch to the synthesis and secretion of IgE antibodies?

T H 2 lymphocytes that help B lymphocytes switch to the synthesis and secretion of IgE antibodies.