Immune system acquired

Human Immunodeficiency Virus. Human immunodeficiency vims (HIV) causes Acquired Immunodeficiency Syndrome (AIDS), which has no cure. HIV infects the cells of the human immune system, such as T-lymphocytes, monocytes, and macrophages. After a long period of latency and persistent infection, it results in the progressive decline of the immune system, and leads to full-blown AIDS, resulting in death. 

AIDS (acquired immunodeficiency syndrome) is the final stage of disease caused by infection with HIV. In this stage, the vims infection has severely affected the immune system, causing a depletion of CD4+ T-helper cells. AIDS is characterized by the manifestation of typical diseases caused by opportunistic infections (Pneumocystis carinii pneumonia, CMV retinitis, candidiasis of the esophagus, cerebral toxoplasmosis), neurological manifestations, cachexia, or certain tumors (Kaposi sarcoma of the skin, B-cell lymphoma). 

However, several situations can be anticipated in which support of the immune system is required. These include congenital defects in the immune repertoire, acquired immune deficiencies such as in HIV infection, but also situations in which the immune system is compromised after treatment of patients, e.g., after radiation or chemotherapy. 

These disorders are all acquired conditions with no evidence of an hereditary basis. Most of them involve inflammation of the skeletal muscle itself (myositis) (Figure 17), though this may sometimes occur because of initial targeting of the muscle vasculature or connective tissue. Many instances of myositis are classed as idiopathic disorders, in that the precise mechanisms of muscle degeneration are not known, but is widely accepted that these syndromes are associated with abnormal function of the immune system. The syndromes of polymyositis (PM) and derma-... 

Infection with a human immunodeficiency virus (HIV-1 and HIV-2 see Chapter 3) can cause the destruction of the TH cell, which is the eritieal eell of the immune system. This leads to the condition known as acquired immune deficieney syndrome (AIDS). At present, it is still not known why, in some cases, infection with HIV leaves the immune system intact whereas in others it is irreversibly destroyed, giving rise to AIDS. 

The acquired immune deficiency syndrome (AIDS) was first recognized in 1981, and described in a cohort of young homosexual men with significant immune deficiency. Since then, human immunodeficiency virus type 1 (HIV-1) has been clearly identified as the major cause of AIDS.1 HIV-2 is much less prevalent than HIV-1, but also causes AIDS. HIV primarily targets CD4+ lymphocytes, which are critical to proper immune system function. If left untreated, patients experience a prolonged asymptomatic period followed by rapid, progressive immunodeficiency. Therefore, most complications experienced by patients with AIDS involve opportunistic infections and cancers. 

Inflammation is the normal host response to infection or injury that mediates immune elimination of pathogens and tissue repair. Inflammatory processes include increased production of cytokines, chemokines, nitric oxide, and eicosanoids by the innate immune system in conjunction with altered leukocyte homing, all of which greatly impact acquired immunity. Aberrant inflammatory responses evoke both acute injury such... 

Rodent and human immunology has served to guide our understanding of the mammalian immune system, where the highly conserved innate immune system, and the more complex acquired or adaptive immune system, interact to protect the host from infection. 

The acquired immune system has probably received most of the attention in marine mammals, as has been the case in rodent and human immunology. Recent advances include the production of monoclonal [22-24] and polyclonal [25] antibodies to marine mammal immunoglobulins, enabling more precise, and often species-specific, reagents for the detection and quantification of antigen-specific antibodies. 

Lymphocytes, the effector cells of the acquired immune system, include morphologically indistinguishable T and B cells, the former divided into CD4+ T helper cells and CD8+ cytotoxic T cells. Since the functions of those cell subsets differ so drastically, it became important to develop tools to distinguish them from each other. Efforts to identify cell subsets according to their expression of different surface antigens have been successful, including various Cluster of Determination (CD) markers (Table 23.1). In addition, cross-reactive monoclonal antibodies, and subsequently developed species-specific polyclonal and monoclonal antibodies towards the major histocompatibility complex (MHC) have been used to label cells in circulation and in tissue sections (Table 23.1). 

Other cell-surface molecules important to the acquired immune system have been characterized at the molecular level, including beluga whale CD4 [26], bottlenose... 

In addition to being able to recognize the different cells involved in the acquired immune system of marine mammals, it is important to assure that the cells perform their functions appropriately. The ability of lymphocytes to proliferate upon stimulation (usually with mitogens) has been studied for several decades [1,12,14,15, 32-35], Recent advances include the demonstration of a conserved specificity for standard mitogens used in beluga whales [32] and harbor seals [33], An assay to assess the expression of the receptor for interleukin-2 (IL-2), an early event in lymphocyte activation, was adapted in harbor seals [35], bottlenose dolphins [36], and sea otters [37], Molecular and biochemical mechanisms of activation of beluga T lymphocytes do not vary substantially from those in other mammals [38],... 

Similarly, under certain disease conditions, altered NA innervation and/or AR signaling capacity impairs sympathetic communication with cells of the immune system, influencing disease progression. Altered catecholamine communication with the immune system is evident in autoimmune diseases such as arthritis and multiple sclerosis [5-7] and in infectious diseases, such as leprosy and a mouse model of acquired immunodeficiency syndrome [15, 43, 44], The impact of altered NA innervation of... 

Thus, these data indicate that similar to immature DCs, alternatively activated MO can induce immunosuppressive Tregs and that in return these Tregs are potent suppressors of MO maturation (fig. 2). Since MO bridge the innate and the acquired immune system, Tregs are able to gain influence on the innate immune system by interactions with MO. 

In conclusion, the mutual interaction of Tregs and APCs enables Tregs to sustain their immunosuppressive function(s), which may be crucial for the maintenance of peripheral tolerance in healthy individuals. Since MO and DCs bridge the innate and the acquired immune system, this crosstalk with MO and DCs permits Tregs to gain influence on the iimate immune system. Furthermore, the impact on APCs offers Tregs to expand their suppression beyond the mere interaction with effector T cells. 

Immune systems in animals and plants are quite different. There are two types of immune systems in animals (1) innate, so-called non-specific or passive immunity (2) adaptive, so-called specifically acquired , active, or cell-mediated immunity. Innate immunity is based on barriers to infectious agents and adaptive immunity is based on multiplicative and specific antibody release after contact with an antigen (infectious agent). The so-called memory cells in animals respond to secondary contact with an antigen. 

Components of the maternal innate and acquired immune system... 

Human immunodeficiency virus (HIV)— Virus that causes AIDS (acquired immunodeficiency syndrome) by destroying a critical cell of the body s immune system. 

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