Autoimmunity is the system of immune responses of an organism against
its own healthy cells and tissues. Any disease that results from such
an aberrant immune response is termed an "autoimmune disease".
Prominent examples include celiac disease, diabetes mellitus type 1,
sarcoidosis, systemic lupus erythematosus (SLE), Sjögren's syndrome,
eosinophilic granulomatosis with polyangiitis, Hashimoto's
thyroiditis, Graves' disease, idiopathic thrombocytopenic purpura,
Addison's disease, rheumatoid arthritis (RA), ankylosing spondylitis,
polymyositis (PM), dermatomyositis (DM) and multiple sclerosis (MS).
Autoimmune diseases are very often treated with steroids.
2 Low-level autoimmunity
3 Immunological tolerance
Immunodeficiency and autoimmunity
5 Genetic factors
7 Environmental factors
8 Pathogenesis of autoimmunity
11.1 Nutrition and autoimmunity
12 See also
14 External links
In the later 19th century it was believed that the immune system was
unable to react against the body's own tissues. Paul Ehrlich, at the
turn of the 20th century, proposed the concept of horror autotoxicus.
Ehrlich later adjusted his theory to recognize the possibility of
autoimmune tissue attacks, but believed certain innate protection
mechanisms would prevent the autoimmune response from becoming
In 1904 this theory was challenged by the discovery of a substance in
the serum of patients with paroxysmal cold hemoglobinuria that reacted
with red blood cells. During the following decades, a number of
conditions could be linked to autoimmune responses. However, the
authoritative status of Ehrlich's postulate hampered the understanding
of these findings.
Immunology became a biochemical rather than a
clinical discipline. By the 1950s the modern understanding of
autoantibodies and autoimmune diseases started to spread.
More recently it has become accepted that autoimmune responses are an
integral part of vertebrate immune systems (sometimes termed "natural
autoimmunity"), normally prevented from causing disease by the
phenomenon of immunological tolerance to self-antigens.[citation
Autoimmunity should not be confused with alloimmunity.
While a high level of autoimmunity is unhealthy, a low level of
autoimmunity may actually be beneficial. Taking the experience of a
beneficial factor in autoimmunity further, one might hypothesize with
intent to prove that autoimmunity is always a self-defense mechanism
of the mammal system to survive. The system does not randomly lose the
ability to distinguish between self and non-self, the attack on cells
may be the consequence of cycling metabolic processes necessary to
keep the blood chemistry in homeostasis.
Second, autoimmunity may have a role in allowing a rapid immune
response in the early stages of an infection when the availability of
foreign antigens limits the response (i.e., when there are few
pathogens present). In their study, Stefanova et al. (2002) injected
MHC Class II
MHC Class II antibody into mice expressing a single type of
MHC Class II
MHC Class II molecule (H-2b) to temporarily prevent CD4+ T cell-MHC
CD4+ T cells
CD4+ T cells (those that have not encountered any
antigens before) recovered from these mice 36 hours post-anti-MHC
administration showed decreased responsiveness to the antigen pigeon
cytochrome C peptide, as determined by
Interleukin-2 production. Thus Stefanova et al.
(2002) demonstrated that self-MHC recognition (which, if too strong
may contribute to autoimmune disease) maintains the responsiveness of
CD4+ T cells
CD4+ T cells when foreign antigens are absent. This idea of
autoimmunity is conceptually similar to play-fighting. The
play-fighting of young cubs (TCR and self-MHC) may result in a few
scratches or scars (low-level-autoimmunity), but is beneficial in the
long-term as it primes the young cub for proper fights in the future.
Pioneering work by Noel Rose and
Ernst Witebsky in New York, and Roitt
and Doniach at
University College London
University College London provided clear evidence that,
at least in terms of antibody-producing B cells (B lymphocytes),
diseases such as rheumatoid arthritis and thyrotoxicosis are
associated with loss of immunological tolerance, which is the ability
of an individual to ignore "self", while reacting to "non-self". This
breakage leads to the immune system's mounting an effective and
specific immune response against self determinants. The exact genesis
of immunological tolerance is still elusive, but several theories have
been proposed since the mid-twentieth century to explain its origin.
Three hypotheses have gained widespread attention among immunologists:
Clonal Deletion theory, proposed by Burnet, according to which
self-reactive lymphoid cells are destroyed during the development of
the immune system in an individual. For their work Frank M. Burnet and
Peter B. Medawar were awarded the 1960 Nobel Prize in Physiology or
Medicine "for discovery of acquired immunological tolerance".
Clonal Anergy theory, proposed by Nossal, in which self-reactive T- or
B-cells become inactivated in the normal individual and cannot amplify
the immune response.
Idiotype Network theory, proposed by Jerne, wherein a network of
antibodies capable of neutralizing self-reactive antibodies exists
naturally within the body.
In addition, two other theories are under intense investigation:
Clonal Ignorance theory, according to which autoreactive T cells that
are not represented in the thymus will mature and migrate to the
periphery, where they will not encounter the appropriate antigen
because it is inaccessible tissues. Consequently, auto-reactive B
cells, that escape deletion, cannot find the antigen or the specific
helper T cell.
Suppressor population or
Regulatory T cell
Regulatory T cell theory, wherein regulatory
T-lymphocytes (commonly CD4+FoxP3+ cells, among others) function to
prevent, downregulate, or limit autoaggressive immune responses in the
Tolerance can also be differentiated into "Central" and "Peripheral"
tolerance, on whether or not the above-stated checking mechanisms
operate in the central lymphoid organs (Thymus and Bone Marrow) or the
peripheral lymphoid organs (lymph node, spleen, etc., where
B-cells may be destroyed). It must be emphasised that
these theories are not mutually exclusive, and evidence has been
mounting suggesting that all of these mechanisms may actively
contribute to vertebrate immunological tolerance.
A puzzling feature of the documented loss of tolerance seen in
spontaneous human autoimmunity is that it is almost entirely
restricted to the autoantibody responses produced by B lymphocytes.
Loss of tolerance by T cells has been extremely hard to demonstrate,
and where there is evidence for an abnormal
T cell response it is
usually not to the antigen recognised by autoantibodies. Thus, in
rheumatoid arthritis there are autoantibodies to IgG Fc but apparently
T cell response. In systemic lupus there are
autoantibodies to DNA, which cannot evoke a
T cell response, and
limited evidence for
T cell responses implicates nucleoprotein
Celiac disease there are autoantibodies to tissue
transglutaminase but the
T cell response is to the foreign protein
gliadin. This disparity has led to the idea that human autoimmune
disease is in most cases (with probable exceptions including type I
diabetes) based on a loss of
B cell tolerance which makes use of
T cell responses to foreign antigens in a variety of aberrant
Immunodeficiency and autoimmunity
There are a large number of immunodeficiency syndromes that present
clinical and laboratory characteristics of autoimmunity. The decreased
ability of the immune system to clear infections in these patients may
be responsible for causing autoimmunity through perpetual immune
One example is common variable immunodeficiency (CVID) where multiple
autoimmune diseases are seen, e.g.: inflammatory bowel disease,
autoimmune thrombocytopenia and autoimmune thyroid disease.
Familial hemophagocytic lymphohistiocytosis, an autosomal recessive
primary immunodeficiency, is another example. Pancytopenia, rashes,
swollen lymph nodes and enlargement of the liver and spleen are
commonly seen in such individuals. Presence of multiple uncleared
viral infections due to lack of perforin are thought to be
In addition to chronic and/or recurrent infections many autoimmune
diseases including arthritis, autoimmune hemolytic anemia, scleroderma
and type 1 diabetes mellitus are also seen in X-linked
agammaglobulinemia (XLA). Recurrent bacterial and fungal infections
and chronic inflammation of the gut and lungs are seen in chronic
granulomatous disease (CGD) as well. CGD is a caused by decreased
production of nicotinamide adenine dinucleotide phosphate (NADPH)
oxidase by neutrophils. Hypomorphic RAG mutations are seen in patients
with midline granulomatous disease; an autoimmune disorder that is
commonly seen in patients with granulomatosis with polyangiitis
(formerly known as Wegener’s granulomatosis) and NK/T cell
Wiskott-Aldrich syndrome (WAS) patients also present with eczema,
autoimmune manifestations, recurrent bacterial infections and
In autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy
(APECED) also autoimmunity and infections coexist: organ-specific
autoimmune manifestations (e.g. hypoparathyroidism and adrenocortical
failure) and chronic mucocutaneous candidiasis.
IgA deficiency is also sometimes associated with the
development of autoimmune and atopic phenomena.
Certain individuals are genetically susceptible to developing
autoimmune diseases. This susceptibility is associated with multiple
genes plus other risk factors. Genetically predisposed individuals do
not always develop autoimmune diseases.
Three main sets of genes are suspected in many autoimmune diseases.
These genes are related to:
The major histocompatibility complexes (MHC).
The first two, which are involved in the recognition of antigens, are
inherently variable and susceptible to recombination. These variations
enable the immune system to respond to a very wide variety of
invaders, but may also give rise to lymphocytes capable of
Scientists such as Hugh McDevitt, G. Nepom, J. Bell and J. Todd have
also provided strong evidence to suggest that certain MHC class II
allotypes are strongly correlated with[clarification needed][citation
HLA DR2 is strongly positively correlated with Systemic Lupus
Erythematosus, narcolepsy and multiple sclerosis, and negatively
correlated with DM Type 1.
HLA DR3 is correlated strongly with Sjögren's syndrome, myasthenia
gravis, SLE, and DM Type 1.
HLA DR4 is correlated with the genesis of rheumatoid arthritis, Type 1
diabetes mellitus, and pemphigus vulgaris.
Fewer correlations exist with MHC class I molecules. The most notable
and consistent is the association between HLA B27 and
spondyloarthropathies like ankylosing spondylitis and reactive
arthritis. Correlations may exist between polymorphisms within class
II MHC promoters and autoimmune disease.
The contributions of genes outside the MHC complex remain the subject
of research, in animal models of disease (Linda Wicker's extensive
genetic studies of diabetes in the NOD mouse), and in patients (Brian
Kotzin's linkage analysis of susceptibility to SLE).
PTPN22 has been associated with multiple autoimmune diseases
including Type I diabetes, rheumatoid arthritis, systemic lupus
erythematosus, Hashimoto’s thyroiditis, Graves’ disease,
Addison’s disease, Myasthenia Gravis, vitiligo, systemic sclerosis
juvenile idiopathic arthritis, and psoriatic
Ratio of female/male incidence
of autoimmune diseases
Multiple sclerosis (MS)
Systemic lupus erythematosus
Systemic lupus erythematosus (SLE)
Primary sclerosing cholangitis
A person's sex also seems to have some role in the development of
autoimmunity; that is, most autoimmune diseases are sex-related.
Nearly 75% of the more than 23.5 million Americans who suffer from
autoimmune disease are women, although it is less-frequently
acknowledged that millions of men also suffer from these diseases.
According to the American Autoimmune Related Diseases Association
(AARDA), autoimmune diseases that develop in men tend to be more
severe. A few autoimmune diseases that men are just as or more likely
to develop as women include: ankylosing spondylitis, type 1 diabetes
mellitus, granulomatosis with polyangiitis, Crohn's disease, Primary
sclerosing cholangitis and psoriasis.
The reasons for the sex role in autoimmunity vary. Women appear to
generally mount larger inflammatory responses than men when their
immune systems are triggered, increasing the risk of autoimmunity.
Involvement of sex steroids is indicated by that many autoimmune
diseases tend to fluctuate in accordance with hormonal changes, for
example: during pregnancy, in the menstrual cycle, or when using oral
contraception. A history of pregnancy also appears to leave a
persistent increased risk for autoimmune disease. It has been
suggested that the slight, direct exchange of cells between mothers
and their children during pregnancy may induce autoimmunity. This
would tip the gender balance in the direction of the female.
Another theory suggests the female high tendency to get autoimmunity
is due to an imbalanced X chromosome inactivation. The
X-inactivation skew theory, proposed by Princeton University's Jeff
Stewart, has recently been confirmed experimentally in scleroderma and
autoimmune thyroiditis. Other complex X-linked genetic
susceptibility mechanisms are proposed and under investigation.
An interesting inverse relationship exists between infectious diseases
and autoimmune diseases. In areas where multiple infectious diseases
are endemic, autoimmune diseases are quite rarely seen. The reverse,
to some extent, seems to hold true. The hygiene hypothesis attributes
these correlations to the immune manipulating strategies of pathogens.
While such an observation has been variously termed as spurious and
ineffective, according to some studies, parasite infection is
associated with reduced activity of autoimmune disease.
The putative mechanism is that the parasite attenuates the host immune
response in order to protect itself. This may provide a serendipitous
benefit to a host that also suffers from autoimmune disease. The
details of parasite immune modulation are not yet known, but may
include secretion of anti-inflammatory agents or interference with the
host immune signaling.
A paradoxical observation has been the strong association of certain
microbial organisms with autoimmune diseases. For example, Klebsiella
pneumoniae and coxsackievirus B have been strongly correlated with
ankylosing spondylitis and diabetes mellitus type 1, respectively.
This has been explained by the tendency of the infecting organism to
produce super-antigens that are capable of polyclonal activation of
B-lymphocytes, and production of large amounts of antibodies of
varying specificities, some of which may be self-reactive (see below).
Certain chemical agents and drugs can also be associated with the
genesis of autoimmune conditions, or conditions that simulate
autoimmune diseases. The most striking of these is the drug-induced
lupus erythematosus. Usually, withdrawal of the offending drug cures
the symptoms in a patient.
Cigarette smoking is now established as a major risk factor for both
incidence and severity of rheumatoid arthritis. This may relate to
abnormal citrullination of proteins, since the effects of smoking
correlate with the presence of antibodies to citrullinated peptides.
Pathogenesis of autoimmunity
Several mechanisms are thought to be operative in the pathogenesis of
autoimmune diseases, against a backdrop of genetic predisposition and
environmental modulation. It is beyond the scope of this article to
discuss each of these mechanisms exhaustively, but a summary of some
of the important mechanisms have been described:
T-Cell Bypass – A normal immune system requires the activation of
T-cells before the former can undergo differentiation into
B-cells and subsequently produce antibodies in large
quantities. This requirement of a T-cell can be bypassed in rare
instances, such as infection by organisms producing super-antigens,
which are capable of initiating polyclonal activation of B-cells, or
even of T-cells, by directly binding to the β-subunit of T-cell
receptors in a non-specific fashion.
T-Cell-B-Cell discordance – A normal immune response is assumed to
involve B and
T cell responses to the same antigen, even if we know
that B cells and T cells recognise very different things:
conformations on the surface of a molecule for B cells and
pre-processed peptide fragments of proteins for T cells. However,
there is nothing as far as we know that requires this. All that is
required is that a
B cell recognising antigen X endocytoses and
processes a protein Y (normally =X) and presents it to a T cell.
Roosnek and Lanzavecchia showed that B cells recognising IgGFc could
get help from any
T cell responding to an antigen co-endocytosed with
IgG by the
B cell as part of an immune complex. In coeliac disease it
seems likely that B cells recognising tissue transglutamine are helped
by T cells recognising gliadin.
B cell receptor-mediated feedback – A feature of human
autoimmune disease is that it is largely restricted to a small group
of antigens, several of which have known signaling roles in the immune
response (DNA, C1q, IgGFc, Ro, Con. A receptor, Peanut agglutinin
receptor(PNAR)). This fact gave rise to the idea that spontaneous
autoimmunity may result when the binding of antibody to certain
antigens leads to aberrant signals being fed back to parent B cells
through membrane bound ligands. These ligands include
B cell receptor
(for antigen), IgG Fc receptors, CD21, which binds complement C3d,
Toll-like receptors 9 and 7 (which can bind DNA and nucleoproteins)
and PNAR. More indirect aberrant activation of B cells can also be
envisaged with autoantibodies to acetyl choline receptor (on thymic
myoid cells) and hormone and hormone binding proteins. Together with
the concept of T-cell-B-cell discordance this idea forms the basis of
the hypothesis of self-perpetuating autoreactive B cells.
Autoreactive B cells in spontaneous autoimmunity are seen as surviving
because of subversion both of the
T cell help pathway and of the
feedback signal through
B cell receptor, thereby overcoming the
negative signals responsible for
B cell self-tolerance without
necessarily requiring loss of
T cell self-tolerance.
Molecular Mimicry – An exogenous antigen may share structural
similarities with certain host antigens; thus, any antibody produced
against this antigen (which mimics the self-antigens) can also, in
theory, bind to the host antigens, and amplify the immune response.
The idea of molecular mimicry arose in the context of Rheumatic Fever,
which follows infection with Group A beta-haemolytic streptococci.
Although rheumatic fever has been attributed to molecular mimicry for
half a century no antigen has been formally identified (if anything
too many have been proposed). Moreover, the complex tissue
distribution of the disease (heart, joint, skin, basal ganglia) argues
against a cardiac specific antigen. It remains entirely possible that
the disease is due to e.g. an unusual interaction between immune
complexes, complement components and endothelium.
Idiotype Cross-Reaction –
Idiotypes are antigenic epitopes found in
the antigen-binding portion (Fab) of the immunoglobulin molecule.
Plotz and Oldstone presented evidence that autoimmunity can arise as a
result of a cross-reaction between the idiotype on an antiviral
antibody and a host cell receptor for the virus in question. In this
case, the host-cell receptor is envisioned as an internal image of the
virus, and the anti-idiotype antibodies can react with the host cells.
Cytokine Dysregulation –
Cytokines have been recently divided into
two groups according to the population of cells whose functions they
T-cells type 1 or type 2. The second category of
cytokines, which include IL-4, IL-10 and
TGF-β (to name a few), seem
to have a role in prevention of exaggeration of pro-inflammatory
Dendritic cell apoptosis – immune system cells called dendritic
cells present antigens to active lymphocytes. Dendritic cells that are
defective in apoptosis can lead to inappropriate systemic lymphocyte
activation and consequent decline in self-tolerance.
Epitope spreading or epitope drift – when the immune reaction
changes from targeting the primary epitope to also targeting other
epitopes. In contrast to molecular mimicry, the other epitopes
need not be structurally similar to the primary one.
Epitope modification or Cryptic epitope exposure – this mechanism of
autoimmune disease is unique in that it does not result from a defect
in the hematopoietic system. Instead, disease results from the
exposure of cryptic N-glycan (polysaccharide) linkages common to lower
eukaryotes and prokaryotes on the glycoproteins of mammalian
non-hematopoietic cells and organs This exposure of phylogenically
primitive glycans activates one or more mammalian innate immune cell
receptors to induce a chronic sterile inflammatory state. In the
presence of chronic and inflammatory cell damage, the adaptive immune
system is recruited and self–tolerance is lost with increased
autoantibody production. In this form of the disease, the absence of
lymphocytes can accelerate organ damage, and intravenous IgG
administration can be therapeutic. Although this route to autoimmune
disease may underlie various degenerative disease states, no
diagnostics for this disease mechanism exist at present, and thus its
role in human autoimmunity is currently unknown.
The roles of specialized immunoregulatory cell types, such as
regulatory T cells, NKT cells, γδ
T-cells in the pathogenesis of
autoimmune disease are under investigation.
Autoimmune diseases can be broadly divided into systemic and
organ-specific or localised autoimmune disorders, depending on the
principal clinico-pathologic features of each disease.
Systemic autoimmune diseases
Systemic autoimmune diseases include SLE, Sjögren's syndrome,
sarcoidosis, scleroderma, rheumatoid arthritis, cryoglobulinemic
vasculitis, and dermatomyositis. These conditions tend to be
associated with autoantibodies to antigens which are not tissue
specific. Thus although polymyositis is more or less tissue specific
in presentation, it may be included in this group because the
autoantigens are often ubiquitous t-RNA synthetases.
Local syndromes which affect a specific organ or tissue:
Diabetes mellitus type 1, Hashimoto's thyroiditis,
Gastrointestinal: Coeliac disease, Crohn's disease, Pernicious anaemia
Dermatologic: Pemphigus vulgaris, Vitiligo
Haematologic: Autoimmune haemolytic anaemia, Idiopathic
Neurological: Multiple sclerosis, Myasthenia gravis, Encephalitis
Using the traditional “organ specific” and “non-organ
specific” classification scheme, many diseases have been lumped
together under the autoimmune disease umbrella. However, many chronic
inflammatory human disorders lack the telltale associations of B and T
cell driven immunopathology. In the last decade it has been firmly
established that tissue "inflammation against self" does not
necessarily rely on abnormal T and
B cell responses.
This has led to the recent proposal that the spectrum of autoimmunity
should be viewed along an “immunological disease continuum,” with
classical autoimmune diseases at one extreme and diseases driven by
the innate immune system at the other extreme. Within this scheme, the
full spectrum of autoimmunity can be included. Many common human
autoimmune diseases can be seen to have a substantial innate immune
mediated immunopathology using this new scheme. This new
classification scheme has implications for understanding disease
mechanisms and for therapy development.
Diagnosis of autoimmune disorders largely rests on accurate history
and physical examination of the patient, and high index of suspicion
against a backdrop of certain abnormalities in routine laboratory
tests (example, elevated C-reactive protein). In several systemic
disorders, serological assays which can detect specific autoantibodies
can be employed. Localised disorders are best diagnosed by
immunofluorescence of biopsy specimens.
Autoantibodies are used to
diagnose many autoimmune diseases. The levels of autoantibodies are
measured to determine the progress of the disease.
Treatments for autoimmune disease have traditionally been
immunosuppressive, anti-inflammatory, or palliative. Managing
inflammation is critical in autoimmune diseases. Non-immunological
therapies, such as hormone replacement in
Hashimoto's thyroiditis or
Type 1 diabetes mellitus
Type 1 diabetes mellitus treat outcomes of the autoaggressive
response, thus these are palliative treatments. Dietary manipulation
limits the severity of celiac disease. Steroidal or NSAID treatment
limits inflammatory symptoms of many diseases. IVIG is used for CIDP
and GBS. Specific immunomodulatory therapies, such as the TNFα
antagonists (e.g. etanercept), the
B cell depleting agent rituximab,
the anti-IL-6 receptor tocilizumab and the costimulation blocker
abatacept have been shown to be useful in treating RA. Some of these
immunotherapies may be associated with increased risk of adverse
effects, such as susceptibility to infection.
Helminthic therapy is an experimental approach that involves
inoculation of the patient with specific parasitic intestinal
nematodes (helminths). There are currently two closely related
treatments available, inoculation with either Necator americanus,
commonly known as hookworms, or Trichuris Suis Ova, commonly known as
Pig Whipworm Eggs.
T cell vaccination is also being explored as a possible future therapy
for autoimmune disorders.
Nutrition and autoimmunity
Because most human cells and tissues have receptors for vitamin D,
including T and B cells, adequate levels of vitamin D can aid in the
regulation of the immune system. Vitamin D plays a role in immune
function by acting on T cells and natural
killer cells. Research has demonstrated an association
between low serum vitamin D and autoimmune diseases,
including multiple sclerosis, type 1 diabetes,
and Systemic Lupus Erythematosus (commonly referred to
simply as lupus). However,
since photosensitivity occurs in lupus, patients are advised
to avoid sunlight which may be responsible for vitamin D deficiency
seen in this disease. Polymorphisms in
the vitamin D receptor gene are commonly found in people
with autoimmune diseases, giving one potential mechanism for vitamin
D's role in autoimmunity. There is mixed evidence on the
effect of vitamin D supplementation in type 1 diabetes, lupus, and
Omega-3 Fatty Acids
Studies have shown that adequate consumption of omega-3 fatty acids
counteracts the effects of arachidonic acids, which contribute to
symptoms of autoimmune diseases. Human and animal trials suggest that
omega-3 is an effective treatment modality for many cases of
Rheumatoid Arthritis, Inflammatory Bowel Disease, Asthma, and
While major depression is not necessarily an autoimmune disease, some
of its physiological symptoms are inflammatory and autoimmune in
nature. Omega-3 may inhibit production of interferon gamma and other
cytokines which cause the physiological symptoms of depression. This
may be due to the fact that an imbalance in omega-3 and omega-6 fatty
acids, which have opposing effects, is instrumental in the etiology of
Various types of bacteria and microflora present in fermented dairy
products, especially Lactobacillus casei, have been shown to both
stimulate immune response to tumors in mice and to regulate immune
function, delaying or preventing the onset of nonobese diabetes. This
is particularly true of the Shirota strain of L. casei (LcS). The LcS
strain is mainly found in yogurt and similar products in Europe and
Japan, and rarely elsewhere.
It has been theorized that free radicals contribute to the onset of
type-1 diabetes in infants and young children, and therefore that the
risk could be reduced by high intake of antioxidant substances during
pregnancy. However, a study conducted in a hospital in Finland from
1997-2002 concluded that there was no statistically significant
correlation between antioxidant intake and diabetes risk. This
study involved monitoring of food intake through questionnaires, and
estimated antioxidant intake on this basis, rather than by exact
measurements or use of supplements.
Systemic autoimmune disease
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American Autoimmune Related Diseases Association: a nonprofit advocacy
Immune Tolerance Network: a research-oriented resource
Nobel Prize The 1960 Nobel Prize in Physiology or Medicine was awarded
to Frank M. Burnet and Peter B Medawar.
Autoimmunity can be caused by environmental toxins
Immunology Database and Analysis
Portal – an NIAID-funded
database resource of reference and experiment data covering the entire
Autoimmunity Conference - Leading scientists meet to enrich their
knowledge with guest lecturers and advanced courses.
Understanding Autoimmune Diseases - US National Institute of
Arthritis and Musculoskeletal and Skin Diseases
Immunology: lymphocytic adaptive immune system and complement
Antigen presentation/Professional APCs: Dendritic cell
B cell response
Tolerance in pregnancy
Immunoglobulin class switching
Hypersensitivity and autoimmune diseases (279.5–6)
Allergic rhinitis (Hay fever)
common allergies include: Milk
Hemolytic disease of the newborn
Autoimmune hemolytic anemia
Immune thrombocytopenic purpura
Systemic lupus erythematosus
Subacute bacterial endocarditis
Allergic contact dermatitis
Diabetes mellitus type 1
Postorgasmic illness syndrome
Transfusion-associated graft versus host disease
Allergic bronchopulmonary aspergillosis
Latex allergy (I+IV)
Autoimmune polyendocrine syndrome