Filtrate that enters the renal corpuscle in Bowman’s capsule is forced in due to hydrostatic blood pressure; this is a passive mechanism. However, as the filtrate is reabsorbed in the proximal convoluted tubule (PCT), some molecules exit the tubule via active transport mechanisms. Later, as filtrate travels through the descending limb of the loop of Henle, water moves out passively with its concentration gradient, as do sodium ions in the thin ascending limb. In the thick ascending limb, the concentration of salt has increased in the medulla, causing salt to exit the tubule via active transport mechanisms. Finally, in the distal convoluted tubule and collecting duct, water reabsorption occurs passively through aquaporins, but some reabsorption and secretion may occur through active transport.

Active transport occurs in the proximal convoluted tubule, ascending loop of Henle, distal convoluted tubule, and collecting duct.

Renin is released from these cells in response to decreased arteriole blood pressure. The renin-angiotensin-aldosterone system is then activated to maintain blood pressure by various ways including stimulating thirst, reabsorbing sodium in the kidney, and increasing vasopressin release.

Aldosterone is released by the adrenal glands and works to increase sodium retention which increases water retention and thereby increases blood volume to increase blood pressure. If sodium flows back into the cells from the kidney tubules (so that it is not secreted as urine), water also flows back as an osmotic effect. Additionally, aldosterone also stimulates thirst and decreases vasopressin secretion, all to increase blood volume to increase blood pressure.

The spleen is like a giant lymph node, and it is organized in a somewhat similar manner. Although it can be surgically removed if it is damaged, such patients are at life-long risk of death from fairly ordinary infectious processes. The spleen is a reservoir of immune competence. Blood passes through the spleen for exposure to white blood cells. When the white blood cells detect antigens or foreign particles in the blood, they initiate the immune response. The spleen is essentially a screening center to check the blood for contaminants.

Adaptive immunity occurs when antibodies are produced as a result of exposure to a pathogen or immunization. These antibodies are specific for the particular microorganism and memory cells are produced. Cell-mediated immunity is a direct form of defense based on the action of lymphocytes to attack foreign cells and destroy them. Congenital immunity is immunity one is born with. This may result from antibodies received from the mother's blood. Innate immunity is not pathogen-specific and includes the secretion of proteins and the activities of natural killer cells. Passive immunity involves the introduction of preformed antibodies into an unprotected individual. This may occur through infusion of immune globulin or antibodies that pass from the mother to the fetus through the placenta.

VDJ recombination occurs during early B- and T-cell maturation, resulting in diverse antibodies and T-cells. This DNA recombination occurs between the V, D, and J segments of the antibody or T-cell before transcription occurs. As a result, a unique sequence is generated, transcribed, and then translated to a functional protein. This recombination is responsible for creating the unique series of antibodies that the body is capable of producing in order to detect the various antigens represented by foreign pathogens.

B cells and T cells are both part of the adaptive immunity. B cells secrete antibodies that bind to foreign antigens. Upon binding to a specific antigen, B cells can be activated by T cells, which facilitate the synthesis of specific antibodies for the antigen. This enhances the antibody-antigen binding and allows for a better immune response. T cells have receptors on their surface that detect antigens. Once they detect the antigen, T cells can activate B cells and other immune system cells (such as macrophages and neutrophils) to eliminate the foreign antigen. B cells do not play a role in the activation of T cells. 

The question states that the immune complex has antibodies bound to antigens. Recall that B cells eliminate pathogens by secreting antibodies. These antibodies bind to antigens and release factors called cytokines. Cytokines recruit phagocytic cells like macrophages and neutrophils that kill the infected cell. They also activate a part of the innate immune system called the complement, which aids in the elimination of the pathogen. This type of immune response is called a humoral immune response. Elimination of the pathogen using T cells is called a cell-mediated immune response.

Note that both the humoral and the cell-mediated immune responses are very specific responses that are part of the adaptive immunity. Innate immunity involves non-specific immune responses via macrophages, granulocytes (neutrophils, eosinophils, and basophils), complement system, and NK cells.

Plasma cells are circulating cells that form part of adaptive immunity that secrete antibodies to specific antigens. These cells arise from naïve B cells. Broadly specific naïve B cells have the ability to bind to several antigens. Once bound, these naïve B cells differentiate into plasma cells that secrete antibodies that are very specific to the antigen. T cells facilitate this differentiation, but only B cells give rise to plasma cells.

A naïve T cell has the ability to differentiate into three kinds of cells. First, it can differentiate into a helper T cell. These cells facilitate the activation of other immune cells such as B cells, macrophages, and granulocytes. Second, a naïve T cell can differentiate into a cytotoxic T cell. These cells bind to infected cells and induce their death. Third, a naïve T cell can differentiate into a regulatory T cell. These T cells bind to the same antigens as the first two cells; however, instead of initiating an immune response, they regulate it by suppressing the activity of T cells.

HIV is a virus that likes to reside inside helper T cells. A person infected with HIV will have a decreased helper T cell count, which makes the person more susceptible to other opportunistic infections (infections that only occur in immune-compromised individuals). A patient with very low helper T cell count develops AIDS and often passes away due to these opportunistic infections.

There are three kinds of T cells: helper T cells, cytotoxic T cells, and regulatory T cells. All T cells have glycoproteins on their surfaces that act as receptors. CD4 and CD8 are two glycoproteins that can be found on T cells. Helper T cells and regulatory T cells have CD4 glycoproteins, whereas cytotoxic T cells have CD8. These glycoproteins serve as markers to distinguish between T cell types.

The question is asking about CD8, or cytotoxic, T cells. Recall that cytotoxic T cells bind to infected cells and induce their death. Typically, cytotoxic T cells bind to infected cells that have the pathogen inside them (meaning intracellular pathogens). Intracellular pathogens include viruses and intracellular bacteria; therefore, T cells that attack these cells will be CD8 cells. In addition, cytotoxic T cells also attack cancer cells; therefore, these T cells will also be CD8 cells.

Extracellular bacterial cells do not infect host cells; therefore, these bacteria are eliminated via the helper T cells. These T cells bind to the bacteria and activate other immune cells such as B cells, macrophages, and granulocytes that eliminate the bacteria.