**2.1. Acute cellular rejection**

In acute cellular rejection, the antigen-presenting cells directly or indirectly carry the immune message of the graft to the T lymphocyte in a phenomenon known as allorecognition. In this process, the T lymphocyte membrane is bombarded by multiple immune stimuli that activate different effectors, especially calcineurin, which, through interleukin-2, promotes the clonal expansion of T lymphocytes, leading to the production of the following cell clones and enzymes [7, 8].

Auxiliary T lymphocytes (CD4—Helper T lymphocytes) identify antigens on the membrane of cells that have been phagocytosed by macrophages and thereby activate the body's specific immunity;

Cytotoxic T lymphocytes (CD8—Killer T lymphocytes) have the ability to induce lysis of target cells to the case in point the graft cells;

Lymphocytes B are responsible for humoral immunity due to the production of antibodies against foreign antigens, which may give rise to plasma cells (antibody producing cells) or memory cells.

Natural cytotoxic cells (natural killer cells) are granular lymphocytes that destroy target cells by adherence, similar to cytotoxic T lymphocytes (CD8); and the proliferation or rapamycin target enzyme (mTOR—target of rapamycin) regulates the transcription of messenger RNA, acting on growth, proliferation, motility, survival, and protein synthesis of the lymphocyte.

Immunosuppression is generally based on regimens of induction, maintenance, and treatment of acute rejection, described below:

The induction regimen seeks to achieve and induce graft tolerance. This therapy has been reserved for patients at high risk of rejection or renal failure.


## **2.2. Antibody-mediated rejection**

The pathophysiological status, as a consequence of severe cardiomyopathy, is represented by various degrees of systolic and diastolic dysfunction, reflecting low ejection volumes and

Patients in this pathophysiological context also present, among other symptoms, neurohormonal alterations of the renin-angiotensin aldosterone system, decreased renal, visceral, and

The first reference for heart transplantation is from Carrel and Guthrie, who performed the transplantation of an young animal's heart on the neck of an adult animal [3]. It was, however, the work of Lower and Shumway in the 1950s and 1960s that standardized the technique—which provided a long survival for dogs with immunosuppression—and laid the foundations for the success of this surgical treatment. Barnard et al., in 1967, performed the first orthotopic heart transplantation

The presence of high rates of graft rejection and infection accounted for small survival and caused great disinterest and abandonment of the technique in the 70's [5, 6]. However, the experience accumulated by the groups that maintained TxC as a treatment, mainly after the introduction of cyclosporin A, first in kidney transplantation in 1978, and in 1980 in TxC, reinvigorated this therapeutic option, allowing the true development and the application of

In acute cellular rejection, the antigen-presenting cells directly or indirectly carry the immune message of the graft to the T lymphocyte in a phenomenon known as allorecognition. In this process, the T lymphocyte membrane is bombarded by multiple immune stimuli that activate different effectors, especially calcineurin, which, through interleukin-2, promotes the clonal expansion of T lymphocytes, leading to the production of the following cell clones and

Auxiliary T lymphocytes (CD4—Helper T lymphocytes) identify antigens on the membrane of cells that have been phagocytosed by macrophages and thereby activate the body's specific

Cytotoxic T lymphocytes (CD8—Killer T lymphocytes) have the ability to induce lysis of tar-

Lymphocytes B are responsible for humoral immunity due to the production of antibodies against foreign antigens, which may give rise to plasma cells (antibody producing cells) or

Natural cytotoxic cells (natural killer cells) are granular lymphocytes that destroy target cells by adherence, similar to cytotoxic T lymphocytes (CD8); and the proliferation or rapamycin

among humans with relative success, Zerbini being the first to perform it in Brazil [4].

high diastolic volumes and high filling diastolic pressures, respectively [2].

splanchnic perfusion, and increased levels of catecholamines.

**2. Type of rejection in cardiac transplantation**

this treatment worldwide.

172 Heart Transplantation

**2.1. Acute cellular rejection**

get cells to the case in point the graft cells;

enzymes [7, 8].

immunity;

memory cells.

Antibody-mediated rejection can be understood as another form of immune reaction that has a generally more severe course, since circulating preformed antibodies already exists against the alloantigens of the HLA (human leukocyte antigens) graft system. It is a catastrophic situation that leads to acute dysfunction of the organ, and immunosuppressors cannot exert any immediate effect [9–11]. As a preventive measure to curb this event, it has been advocated prior knowledge of the reactivity of the receptor potential to a panel of lymphocytes and the prospective knowledge of cross-lymphocyte testing. In this way, it becomes possible to allocate the donated hearts more rationally to the most suitable recipients.
