Encyclopaedia Britannica, type III hypersensitivity, brain damage

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immune system disorder

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Allergies > Type III hypersensitivity

Type III, or immune-complex, reactions are characterized by tissue damage

caused by the activation of complement in response to _antigen-antibody_

(http://www.britannica.com/eb/topic?idxStructId=28016 & typeId=13) (immune)

complexes

that are deposited in tissues. The classes of antibody involved are the same

ones that participate in type II reactions—IgG and IgM—but the mechanism by

which tissue damage is brought about is different. The antigen to which the

antibody binds is not attached to a cell. Once the antigen-antibody

complexes form, they are deposited in various tissues of the body, especially

the

blood vessels, kidneys, lungs, skin, and joints. Deposition of the immune

complexes causes an inflammatory response, which leads to the release of

tissue-damaging substances, such as enzymes that destroy tissues locally, and

interleukin-1, which, among its other effects, induces fever.

Immune complexes underlie many _autoimmune diseases_

(http://www.britannica.com/eb/article?tocId=215511 & tocid=215511#215511.toc) ,

such as _systemic lupus

erythematosus_ (http://www.britannica.com/eb/article?tocId=9049401) (an

inflammatory disorder of connective tissue), most types of glomerulonephritis

(inflammation of the capillaries of the kidney), and _rheumatoid arthritis_

(http://www.britannica.com/eb/article?tocId=9063421) .

Type III hypersensitivity reactions can be provoked by inhalation of

antigens into the lungs. A number of conditions are attributed to this type of

antigen exposure, including

(http://www.britannica.com/eb/topic?idxStructId=201975 & typeId=13) _farmer's

lung_

(http://www.britannica.com/eb/article?tocId=9033758) , caused by fungal spores

from moldy hay; _pigeon fancier's lung_

(http://www.britannica.com/eb/topic?idxStructId=460152 & typeId=13) , resulting

from

proteins from powdery pigeon dung; and _humidifier fever_

(http://www.britannica.com/eb/topic?idxStructId=276226 & typeId=13) , caused by

normally harmless

protozoans that can grow in air-conditioning units and become dispersed in fine

droplets in climate-controlled offices. In each case, the person will be

sensitized to the antigen—i.e., will have IgG antibodies to the agent

circulating

in the blood. Inhalation of the antigen will stimulate the reaction and

cause chest tightness, fever, and malaise, symptoms that usually pass in a day

or

two but recur when the individual is reexposed to the antigen. Permanent

damage is rare unless individuals are exposed repeatedly. Some occupational

diseases of workers who handle cotton, sugarcane, or coffee waste in warm

countries have a similar cause, with the sensitizing antigen usually coming

from

fungi that grow on the waste rather than the waste itself. The effective

treatment is, of course, to prevent further exposure.

The type of allergy described in the preceding paragraph was first

recognized as (http://www.britannica.com/eb/topic?idxStructId=535915 & typeId=13)

(http://www.britannica.com/eb/article?tocId=9066875) _serum sickness_

(http://www.britannica.com/eb/article?tocId=9066875) , a condition that often

occurred

after animal antiserum had been injected into a patient to destroy _diphtheria_

(http://www.britannica.com/eb/article?tocId=9030572) or _tetanus_

(http://www.britannica.com/eb/article?tocId=9071833) toxins. While still

circulating

in the blood, the foreign proteins in the antiserum induced antibodies, and

some or all of the symptoms described above developed in many subjects. Serum

sickness is now rare, but similar symptoms can develop in people sensitive to

penicillin or certain other drugs, such as _sulfonamides_

(http://www.britannica.com/eb/article?tocId=9070242) . In such cases the drug

combines with the

subject's blood proteins, forming a new antigenic determinant to which

antibodies react.

The consequences of antigen-and-antibody interaction within the bloodstream

vary according to whether the complexes formed are large, in which case they

are usually trapped and removed by macrophages in the liver, spleen, and bone

marrow, or small, in which case they remain in the circulation. Large

complexes occur when more than enough antibody is present to bind to all the

antigen molecules, so that these form aggregates of many antigen molecules

cross-linked together by the multiple binding sites of IgG and IgM antibodies.

When

the ratio of antibody to antigen is enough to form only small complexes, which

can nevertheless activate complement, the complexes tend to settle in the

narrow capillary vessels of the synovial tissue (the lining of joint

cavities), the kidney, the skin, or, less commonly, the brain or the mesentery

of the

gut. The activation of

(http://www.britannica.com/eb/topic?idxStructId=129861 & typeId=13) _complement_

(http://www.britannica.com/eb/article?tocId=9025020) —

which leads to increased permeability of the blood vessels, release of

histamine, stickiness of _platelets_

(http://www.britannica.com/eb/article?tocId=9060348) , and attraction of

granulocytes and macrophages—becomes more

important when the antigen-antibody complexes are deposited in blood vessels

than

when they are deposited in the tissues outside the capillaries. The symptoms,

depending on where the damage occurs, are swollen, painful joints, a raised

skin rash, nephritis (kidney damage, causing blood proteins and even red blood

cells to leak into the urine), diminished blood flow to the brain, or gut

spasms.

The formation of troublesome antigen-antibody complexes in the blood can

also result from subacute

(http://www.britannica.com/eb/topic?idxStructId=48291 & typeId=13) _bacterial

endocarditis_

(http://www.britannica.com/eb/article?tocId=9032612) , a chronic infection of

damaged heart valves. The infectious

agent is often _Streptococcus viridans_

(http://www.britannica.com/eb/topic?idxStructId=568833 & typeId=13) , normally a

harmless inhabitant of the mouth. The

bacteria in the heart become covered with a layer of

(http://www.britannica.com/eb/topic?idxStructId=205873 & typeId=13)

(http://www.britannica.com/eb/article?tocId=9034173) _fibrin_

(http://www.britannica.com/eb/article?tocId=9034173) , which protects them from

destruction by granulocytes, while they continue

to release antigens into the circulation. These can combine with preformed

antibodies to form immune complexes that can cause symptoms resembling those

of serum sickness. Treatment involves eradication of the heart infection by a

prolonged course of antibiotics.