The Immune System


The immune system not only includes the cells, but it also includes the lymphoid structures such as lymph nodes, spleen, tonsils.

The Immune cells

These cells are of two main types: Granulocytes and Agranulocytes. The agranulocytes will be discussed first, particularly the lymphocytes. Lymphocytes are produced from stem cells in the bone marrow. The T cell lymphocytes complete their maturation in the Thymus. B cell lymphocytes are thought to mature in the Bone marrow and are capable of becoming plasma cells. There is also a small group - null cell population - neither B or T - but are natural killer cells. These cells work quickly, with out prior sensitization. However, there activity can be increased by specific lymphokines.

Although B and T cells are morphologically identical, their surface antigens and function help to distinguish which is which. B cells and T cells are programed to respond to specific antigens. B cells to antibody receptor proteins, and T cells to cell surface receptors. Both can act as effector cells, destroying antigens. They also are memory cells, that are capable rapid response to previously encountered antigens. The functions of the macrophages is necessary for B cell and T cell function.


The other major agranculocytes are found as part of the Monocyte/Macrophage system. This was previously referred to as the reticuloendothelial system. Monocyte/Macrophage system includes both mobile and nonmobile phagocytic cells. An example of a nonmobile cell would be kupffer cells in the liver.


The mobile cells, the Monocytes and Macrophages capture antigen, process it, and present antigen to the lymphocytes. The antigen is attached to the outside of the cell and the lymphocyte just "picks it up."


T cells are responsible for the cell mediated immune response. They recognize antigens and release chemotaxic agents to bring other T cells and B cells to the area. The T cells are divided into two groups, regulatory and effector. Both groups are stimulated by antigens to release Lymphokines. (Substances such as interleukin-1 that mediates the inflammatory response including fever, and interferon that protect from intracellular parasites such as viruses. Interferon does this by inhibiting the translation of viral mRNA preventing the production of viral proteins but not normal host cell proteins.)


The regulatory T cells are the helper and suppressor cells that turn-on and turn-off other T cells and the B cells. The effector T cells bind to cell surface antigens on the target cell releasing lymphokines that cause the lysis of the cell membranes of the target cell.


B cells are responsible for humoral immunity. Helper T cells aid the development of B cells into plasma cells. It is plasma cells that produce and secrete immunoglobulins, or antibodies.


Granulocytes are the Neutrophils, Basophils and Eosinophils. These cells can degranulate, releasing their contents as part of the inflammatory response. They are also phagocytic cells.


Immunity and Immune Mechanisms

The immune response describes the interaction between and antigen and an antibody or a reactive T cell.


The antigen-antibody reaction works according to the "lock and key" theory, by its shape and its reactive sites. It is primarily a very specific reaction


Humoral Immunity.

This is mediated by the Complement System, which works in conjunction with antibodies.. This is a collection of plasma proteins, that must be activated in the proper sequence to enable the body to respond to inflammation or infection. This pathway is activated when the target cells evoke an antigen-antibody response. Essentially it is the responses involving specific immunoglobulins, IgG & IgM that initiate complement fixation. The complement system has been shown to influence lysis of cell membranes and coating of the antigen-antibody complex to aid its removal by lymphoid tissue.


Humoral immunity is dependent upon B cells and plasma cell production of immunoglobulins. The primary response occurs when the antigen first enters the body. There is a latent period that is the result of the B cell recognizing the antigen and then producing plasma cells that will produce the necessary antibody. This latent period can last from 48 to 72 hours. After which there is a noticeable rise in antibody titers. Subsequent exposure elicits a faster response with higher antibody titers. (anamestic response)

There are two kinds of plasma cells formed, one produces the antibody, the other becomes a memory cell. The memory cell recognizes the antigen on subsequent infections causing the production of plasma cells that will produce the specific antibody.


Cell Mediated Immunity

Cell mediated immunity involves the actions of T cells and macrophages. Exposure to T cell lymphokines turns the macrophages into very aggressive phagocytes. Activated T cells work by secreting lymphokines and transfer factor. Transfer factor can induce other T cells to secret lymphokines.


Active immunity

Antigen introduced into the host who subsequently activated the activity of immunoglobulin synthesis. Memory


Passive immunity

Injection of preformed immunoglobulin into the host. No Memory for the formation of future antibodies to combat subsequent infections.

These previously mentioned concepts play a major role in maintaining a adequate immune response and in promoting an adequate inflammatory response.


The Inflammatory Response

Inflammation is the local reaction of vascularized tissue to injury. It is necessary in order of wounds to heal and to keep minor infections from becoming overwhelming. The Inflammatory response is closely associated with wound healing and tissue repair.

There are many causes from trauma to infection, however, what ever serves to trigger it, the resulting sequence of events is remarkably similar. The inflammatory response involves a sequence of specific physiologic behaviors that occur in response to injury by a non specific agent. However, the body will only use those behaviors in the sequence that are needed to minimize tissue damage.

Inflammation can be acute or chronic. Acute inflammation is a short lived response associated with all types of tissue injury It involves hemodynamic changes, the formation of an exudate and the presence of granular leukocytes. Chronic inflammation is less uniform and more persistent. It involves the present of nongranular leukocytes and usually results in extensive scar formation.

Acute Inflammation

Rubor (redness), Tumor (swelling), Calor (heat), Dolor (pain), and functio laesa (loss of function)

Vascular Response

Also the hemodynamic response. Momentary constriction of small vessels in the are, followed immediately by vasodilation. The area becomes congested and warm. (Rubor & Calor) There is an increase in capillary permeability, permitting fluid to leak into the interstitial spaces. (Tumor) Toxic and irritating agents are diluted. Plus there is mobilization of the body's defences. Pain and loss of function follow as chemical mediators are released.

Cellular Response

WBC's travel to the area and leave the capillaries as part of the exudate. The leukocytes, marginate along vessel walls, extending pseudopodia to help them move through the walls to get to the source of the inflammation. They are attracted to the source of inflammation or cellular debris by chemotaxis. An affinity for a chemical substance.

The first to arrive are the granulocytes, basically polymorphonuclear leukocytes (polys or neuts). Eos (red stain) (allergic reactions), Basos (Blue stain), Bands, Stabs. The arrival of Basos results in the release of important chemical mediators, Heparin and Histamine. Histamine increases capillary permeability permitting more plasma proteins and fluids to leak into the interstitial spaces. Neutrophils release mediators that serve as chemotaxic agents for monocytes.

Next to arrive are the agranulocytes, the monocytes and lymphocytes. The monocytes are phagocytic cells, often referred to as macrophages, that remove cellular debris and as much of "the invader" as they can. Lymphocytes release lymphokines. mediators that promote chemotaxis of macrophages, neutrophils, and basophils. Other important chemical mediators are bradykinins, which cause increased capillary permeability and pain, and the prostaglandins. Prostaglandins contribute to vasodilation, capillary permeability and the pain and fever of inflammation.

The Monocyte/Macrophage system.

Non mobile phagocytic cells scattered throughout the body. Cells of liver, spleen and lymphoid tissues. These cells ingest the debris of dead cells, bacteria etc. Swollen lymph nodes, and spleen signs of infection.


Inflammatory exudates

Inflammatory exudates are an important part of the process. They enable the necessary supplies to be brought to the site of the inflammation. Initially the exudates consist of plasma proteins, or in the case of allergic rhinitis of serous drainage, dilute, watery exudates low in proteins.

As the inflammatory response progresses, the exudates become fibrous providing fibrinogen and fibrin to build a framework for clot formation or walling off the area to prevent the spread of infection.

Purulent exudates are composed of the remains of WBCs, proteins, and tissue debris. These may be walled off by fibrin and granulation tissue into abscesses.

Resolution of Acute Inflammation

Acute inflammation can be resolved in one of three ways, 1) it can undergo resolution with the injured area returning to normal, 2) it can progress to a purulent (suppurative stage) or 3) it can become chronic.

Chronic Inflammation

Chronic inflammation is self perpetuating and may last for week,s or years. It may develop in the course of a recurrent of progressive acute inflammatory process. This typically occurs with persistent irritants such as talc, and asbestos. These irritants are resistant to phagocytosis and other inflammatory mechanisms. This process usually involves the presence of lymphocytes, plasma cells, and macrophages.


Opportunistic Infections

Immunocompromised patients are at risk for a variety of infections, the most common are CMV, Systemic Fungal infections, Herpes, and Pneumocystis Carinii Pnuemonia (PCP).


PCP is caused by an organism that does not cause infection in healthy individuals. Since it lines the alveolus, it forms a barrier to gaseous exchange. Prior to the development of HIV, it was previously only seen in patients who were immunosuppressed as a result of chemotherapy. The identification of this infection is one of the first clinical criteria in identifying the AIDS disease. Diagnosis is usually made by bronchial lavage. The symptoms may be either gradual or acute. The patient complains of chest pain and sputum production. Clinical findings consist of fever, and increased respiratory rate. Chest X-Ray may show interstitial infiltrates. Approximately 80% of these patients develop respiratory failure. This is the primary reason most AIDS patients are admitted to ICUs. There is severely impaired gaseous exchange. The patients are severely hyoxic and often require intubation and mechanical ventilation. Outcome is varied.


Inflammation & Immunity


Immunity & Disease


Role of Nursing


1) Assessment of immunological data.


2) Identification of the patient 'at risk'.


3) Reverse/Isolation procedures and handwashing.

4) Know which drugs are associated with immunocompromise -Bone marrow suppression.


6) Early Identification of opportunistic infections.