Cyclosporine blocks the activation of T cells by inhibiting the enzyme calcineurin, which is required for the transcription of interleukin-2¹². Interleukin-2 is a cytokine that stimulates the proliferation and differentiation of T cells, which are responsible for recognizing and attacking foreign antigens on the donor organ. By blocking interleukin-2 production, cyclosporine prevents the activation and expansion of T cells, and thus reduces the immune response to the transplanted organ¹³.

The other options are incorrect because:

1. Option A is incorrect because cyclosporine does not inhibit the synthesis of inflammatory mediators or suppress the activation and proliferation of immune cells in general. Cyclosporine is a selective inhibitor of calcineurin, which is mainly involved in T cell activation. Cyclosporine does not affect other inflammatory mediators such as prostaglandins, leukotrienes, or histamine, or other immune cells such as B cells, macrophages, or natural killer cells¹².

C. Option C is incorrect because cyclosporine does not interfere with the synthesis of nucleic acids, which are essential for the replication and function of immune cells. Cyclosporine does not directly affect DNA or RNA synthesis or function, but rather modulates gene expression through its interaction with cyclophilin and calcineurin. Cyclosporine may have some anti-cancer effects by inducing apoptosis or inhibiting angiogenesis in some malignant cells, but this is not its primary mechanism of action¹².

D. Option D is incorrect because cyclosporine does not bind to specific antigens or receptors on the surface of immune cells and either neutralize them or induce their destruction. Cyclosporine acts intracellularly by binding to cyclophilin and inhibiting calcineurin, which are both involved in signal transduction pathways that regulate T cell activation. Cyclosporine does not directly bind to or affect the antigen recognition or receptor-mediated signaling of immune cells¹².

Methylprednisolone is a synthetic glucocorticoid that reduces inflammation, pain, fever, and allergic reactions by inhibiting the synthesis of prostaglandins and leukotrienes¹². Prostaglandins and leukotrienes are lipid-derived inflammatory mediators that are involved in various inflammatory and allergic conditions such as asthma, rheumatoid arthritis, and anaphylaxis. Methylprednisolone inhibits their synthesis by blocking the enzyme cyclooxygenase (COX) and lipoxygenase (LOX), respectively. Methylprednisolone also influences the carbohydrate, protein, and fat metabolism in various tissues, increasing blood glucose and suppressing immune response¹². Methylprednisolone modulates the expression of genes involved in immune regulation, apoptosis, and cell differentiation by interacting with glucocorticoid receptors.

Multiple sclerosis is a chronic autoimmune disease that affects the central nervous system, causing inflammation, demyelination, and axonal damage³. Methylprednisolone is used to treat acute relapses of multiple sclerosis by reducing the inflammation and edema in the brain and spinal cord³. Methylprednisolone may also have some neuroprotective effects by inhibiting the production of reactive oxygen species and nitric oxide, which can cause oxidative stress and neuronal injury³.

The other options are incorrect because:

Option A is incorrect because methylprednisolone does not promote sodium reabsorption and potassium excretion in the kidney, increasing blood volume and blood pressure. This is the effect of mineralocorticoids such as aldosterone, which regulate the fluid and electrolyte balance in the body. Methylprednisolone has a low affinity for mineralocorticoid receptors and does not have significant mineralocorticoid activity¹².

Option C is incorrect because methylprednisolone does not regulate the secretion of adrenocorticotropic hormone (ACTH) from the anterior pituitary gland, maintaining the feedback loop of cortisol production. This is the effect of endogenous glucocorticoids such as cortisol, which are produced by the adrenal cortex in response to ACTH stimulation. Methylprednisolone suppresses the secretion of ACTH from the pituitary gland by negative feedback inhibition, which can lead to adrenal insufficiency if methylprednisolone is discontinued abruptly¹².

Daclizumab is a humanized monoclonal antibody that blocks IL-2 binding by recognizing the interleukin-2 receptor α chain (CD25)¹². CD25 is overexpressed in some leukemias, especially human T-cell leukemia virus 1 associated adult T-cell leukemia/lymphoma (ATL)²³. Daclizumab may have an antileukemic effect by reducing the proliferation and survival of leukemic cells that depend on IL-2 for growth¹³. Daclizumab may also induce antibody-dependent cellular cytotoxicity (ADCC) or complement-dependent cytotoxicity (CDC) against leukemic cells that express CD25¹⁴. Daclizumab may reduce the number and size of malignant cells in the blood and bone marrow, which are the main sites of leukemia¹³.

The other options are incorrect because:

Option A is incorrect because daclizumab does not decrease the frequency and severity of diarrhea, abdominal pain, and rectal bleeding. These are symptoms of ulcerative colitis, a chronic inflammatory bowel disease that affects the colon and rectum. Daclizumab may be used to treat ulcerative colitis by reducing the inflammation and immune-mediated damage to the intestinal mucosa , but this is not its effect in leukemia.

Option B is incorrect because daclizumab does not increase appetite, weight gain, energy level, and quality of life. These are general indicators of health and well-being that may be affected by various factors such as nutrition, physical activity, mental health, social support, and environmental conditions. Daclizumab may improve some aspects of quality of life for patients with leukemia by reducing symptoms and complications of the disease¹³, but this is not a specific outcome of its therapy.

Option C is incorrect because daclizumab does not normalize stool culture, blood count, electrolytes, and liver function tests. These are laboratory tests that measure different aspects of the body's function and health status. Daclizumab may affect some of these tests by causing side effects such as infection, bone marrow suppression, hepatotoxicity, or electrolyte imbalances¹², but this is not an indication of its effectiveness.