Immunopathology

Bagian Patologi Anatomi

Medan - 2015
 An immune response that leads to tissue
injury or disease is broadly called a
hypersensitivity reaction.
Immune, or hypersensitivity-mediated,
diseases are common and include such
entities as hives (urticaria), asthma, hay
fever, hepatitis, glomerulonephritis, and
arthritis.
Type I, or immediate-type hypersensitivity
reactions
IgE antibody is formed and binds to high-
affinity receptors on mast cells and/or
basophils
Subsequent binding of antigen and cross-
linking of IgE trigger rapid (immediate)
release of products from these cells, leading
to the characteristic symptoms of such
diseases as urticaria, asthma, and
anaphylaxis.
Type II hypersensitivity reactions
IgG or IgM antibody is formed against an
antigen, usually a protein on a cell surface.
Less commonly, the antigen is an intrinsic
structural component of the extracellular
matrix (e.g., part of the basement
membrane).
Such antigen-antibody binding activates
complement, which in turn lyses the cell
(cytotoxicity) or damages the extracellular
matrix.
Type III hypersensitivity reactions
The antibody responsible for tissue injury is
also usually IgM or IgG, but the mechanism
of tissue injury differs. The antigen circulates
in the vascular compartment until it is bound
by antibody.
The resulting immune complex is deposited
in tissues. Complement activation at sites of
antigen-antibody deposition leads to
leukocyte recruitment, which is responsible
for the subsequent tissue injury.
Type IV reactions, or cell-mediated, or delayed-
type hypersensitivity reactions
Antigen activation of T lymphocytes, usually
with the help of macrophages, causes
release of products by these cells, thereby
leading to tissue injury.
Many immunologic diseases are mediated by
more than one type of hypersensitivity
reaction. Thus, in hypersensitivity
pneumonitis, lung injury results from
hypersensitivity to inhaled fungal antigens.
Types I, III, and IV hypersensitivity reactions
all appear to be operative in this disease.
 Granulomatous inflammation.
A section of a lymph node shows several granulomas, each made up of an
aggregate of epithelioid cells and surrounded by lymphocytes. The granuloma
in the center shows several multinucleate giant cells.
Autoimmune Disease Involves an Immune
Response Against Self-Antigens
A utoimmunity implies that the immune
system can no longer differentiate between
self- and non-self-antigens effectively.
When these regulatory mechanisms are in
some way disrupted, uncontrolled production
of autoantibodies or abnormal cell, cell
recognition leads to tissue injury, and
autoimmune disease results.
Auto-immune diseases may be organ-specific
or generalized.

Destructive
Rheumatoid Synovitis
SYSTEMIC SCLEROSIS
(SCLERODERMA)
Systemic Lupus Erythematous is a Prototypical
Systemic Immune Complex Disease
Is a chronic, autoimmune, multisystem, inflammatory disease that
may involve almost any organ but characteristically affects
kidneys, joints, serous membranes, and skin.
Autoantibodies are formed against a variety of self-antigens,
including plasma proteins (complement components, clotting
factors) and protein-phospholipid complexes, cell-surface
antigens (lymphocytes, neutrophils, platelets, erythrocytes),
intracellular cytoplasmic components (microfilaments,
microtubules, lysosomes, ribosomes, RNA), and nuclear factors
(DNA, ribonucleoproteins, and histones).
High titers of these two antinuclear antibodies (ANAs) are nearly
pathognomonic of SLE but are not directly cytotoxic. Antigen-
antibody complexes deposit in tissues, leading to the
characteristic vasculitis, synovitis, and glomerulonephritis.
The pathogenesis of systemic lupus erythematosus is
multifactorial. EBV, Epstein-Barr virus; HLA, human
leukocyte antigen
 More than 80% of cases occur in women of childbearing age, as
1 in 700 women
The etiology of SLE is unknown.
Pathology and Clinical Features:
Skin involvement erythematous rash in sun-exposed sites, a
malar butterfly rash being the most characteristic.
Joint disease is the most common manifestation of SLE; more
than 90% of patients have polyarthralgia.
Renal disease, in particular glomerulonephritis

More than one third of patients have pleuritis and pleural effusion.
Pericarditis and peritonitis occur, but less frequently.
Respiratory disorders, ranging from pleural disease to upper
airway involvement and pulmonary parenchymal disease.
Cardiac involvement usually associated with endocarditis,
myocarditis, and pericarditis
Disease of the CNS is a life-threatening complication of lupus.
Vasculitis leading to hemorrhage and infarction of the brain,
which are often lethal.
Antiphospholipid antibodies thromboembolic complications,
including stroke, pulmonary embolism, deep venous thrombosis,
portal vein thrombosis, and spontaneous abortions.
SLE, SKIN SLE, GLOMERULUS
IMMUNE DEFICIENCY DISEASES
Immune deficiency diseases may be caused by inherited
defects affecting immune system development, or they
may result from secondary effects of other diseases
(e.g., infection, malnutrition, aging, immunosuppression,
autoimmunity, or chemotherapy).
Clinically, patients with immune deficiency present with
increased susceptibility to infections as well as to certain
forms of cancer.
The type of infections in a given patient depends largely
on the component of the immune system that is affected.
Patients with defects in Ig, complement, or phagocytic
cells typically suffer from recurrent infections with
pyogenic bacteria, whereas those with defects in cell-
mediated immunity are prone to infections caused by
viruses, fungi, and intracellular bacteria.
AIDS
Etiology: HIV
(SECONDARY IDS)

Pathogenesis: Infection, Latency,

Progressive T-Cell loss
Morphology:

Clinical Expressions: Infections,

Neoplasms, Progressive Immune Failure,
Death, HIV+, HIV-RNA (Viral Load)
Acquired Immunodeficiency Syndrome
AIDS is a retroviral disease caused by the human
immunodeficiency virus (HIV). It is characterized by
infection and depletion of CD4+ T lymphocytes, and
by profound immunosuppression leading to
opportunistic infections, secondary neoplasms, and
neurologic manifestations.
Worldwide, 95% of HIV infections are in developing
countries, with Africa alone carrying more than 50%
of the HIV burden. Although the largest number of
infections is in Africa, the most rapid increases in
HIV infection in the past decade are in Southeast
Asian countries, including Thailand, India, and
Indonesia.
AIDS still represents the fifth most common cause of
death in adults between the ages of 25 and 44.
EPIDEMIOLOGY
HOMOSEXUAL (40%, and
declining)
INTRAVENOUS DRUG USAGE
(25%)
HETEROSEXUAL SEX (10%
and rising)
INFECTIONS
Protozoal/Helminthic:
Cryptosporidium, PCP
(Pneumocystis Carinii
Pneumonia), Toxoplasmosis
Fungal: Candida, and the usual 3

Bacterial: TB, Nocardia,

Salmonella
Viral: CMV, HSV, VZ
Characteristics of antibodies:

IgM: These are the first specific antibodies

in the humoral immune reaction and the main
antibodies in the primary response.
IgA:
This is the main immunoglobulin in bodily
secretions.
In bacterial invasions, the classic role of IgA
antibodies is to activate the complement
system,triggering bacteriolysis and creating a
protective immune layer for the mucous
membranes.
IgG
These normally have the highest serum
concentration of all immunoglobulins.
They play an important role as neutralizing
antibodies in defense against bacterial
infections. In humoral immune reactions, they
replace the IgM antibodies that arrive at the
scene first.
are the main antibodies in the secondary
response and can pass through the placental
barrier.
IgD
: These antibodies often occur together with
IgM
on the surface of B lymphocytes. They
regulate the
interaction between B cells and T cells.
IgE:
These are formed primarily in the MALT
of the respiratory and gastrointestinal tracts
and can attach to mast cells (cytotropic
antibodies).
They also attach to the Langerhans cells that
present antigens.
Anti tumor Effector Mechanisms
Cytotoxic T Lymphocytes
In humans, they seem to play a protective role against
virus-associated neoplasms (e.g., EBV-induced Burkitt
lymphoma and HPV-induced tumors).
Natural Killer Cells
Are lymphocytes that are capable of destroying tumor
cells without prior sensitization; they may provide the first
line of defense against tumor cells after activation with
IL-2.
Macrophages
Activated macrophages may kill tumors by
mechanisms similar to those used to kill microbes
(e.g., production of reactive oxygen metabolites; or
by secretion of tumor necrosis factor (TNF).
Slide Praktikum
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