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2ND YEAR SYSTEMS: Diabetes and Endocrinology > Immunology > Flashcards

Immunology Flashcards

1
Q

How does immunologic tolerance to an antigen happen?

A

When a lymphocyte encounters an antigen it is inactivated or eliminated, leading to tolerance - future exposure to that antigen causes no response

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2
Q

What are antigens that induce tolerance called?

A

Tolerogens

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3
Q

What is meant by the term self-tolerance

A

Tolerance to self antigens

It’s a fundamental property of the normal immune system, and failure of self-tolerance results in immune reactions against self (autologous) antigens.

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4
Q

If reactions occur against self antigens what is this called?

A

Autoimmunity reactions - cause autoimmune diseases

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5
Q

How is autoimmune disease avoided?

A

T and B cells bearing self-reactive molecules must be either eliminated or downregulated so that the immune system is made specifically tolerant to self-antigens.

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6
Q

What mechanisms are involved in making sure the body is tolerant of self-antigens

A

Central (also known as negative selection)

Peripheral

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7
Q

What does a breakdown in any of the immunological tolerance mechanisms cause?

A

Autoimmune responses

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8
Q

By what method can the immune system generate a diversity of T-cell antigen receptors?

A

Differential genetic recombination

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9
Q

Process of central tolerance/negative selection

A

Central tolerance, also known as negative selection, is the process of eliminating any immature T or B lymphocytes that are self-reactive.

3 things happen - apoptosis (deletion), change in receptors or development of Tregs

The thymus plays an important role in eliminating T cells with high affinity to self-antigens

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10
Q

What is important in B cell tolerance?

A

Bone marrow

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11
Q

What is peripheral tolerance

A

Peripheral tolerance is the 2nd branch of immunological tolerance

Comes after central tolerance.

It takes place in the peripheral tissues - some self-reactive mature lymphocytes may enter peripheral tissues and are either inactivated or deleted by encounter with self antigens in these tissues or are suppressed by tregs

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12
Q

What regulates peripheral tolerance? How do they regulate it?

A

regulatory T cells (Tregs)

They actively suppress the activation of lymphocytes specific for self and other antigens

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13
Q

Mechanisms of peripheral tolerance

A

Anergy (functional unresponsiveness)
Treg suppression
Deletion (cell death)

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14
Q

How can you overcome peripheral tolerance/ pre-established tolerance

A

Inappropriate access of self-antigens

Inappropriate or increased local expression of co-stimulatory molecules

Alterations in the ways in which self-molecules are presented to the immune system - structures of self-peptides may be altered by viruses, free radicals or ionising radiation, thus bypassing previously established tolerance.

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15
Q

State 3 factors of tolerance breakdown that may result in autoimmune disease

A

Genes
Infections
Environmental factors

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16
Q

Which gender are almost all types of autoimmune diseases more common in?

A

Females

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17
Q

Non-specific autoimmune diseases

A

They affect multiple organs

Associated with autoimmune responses against self-antigens which are widely distributed throughout the body

Intracellular molecules involved in transcription and translation

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18
Q

Organ specific autoimmune diseases

A

Restricted to one organ

Endocrine glands

19
Q

Self-Antigens binding to TSH receptors or insulin receptors cause what?

A

Hyper or hypo thyroidism

Hyper or hypoglycaemia

20
Q

Self-Antigens binding to acetylcholine receptors causes which disease

A

Myasthenia gravis

21
Q

Epidermal cell adhesion molecules (self-antigens) cause what disease?

A

Blistering skin diseases

22
Q

Self-antigens that are intracellular enzymes and their diseases

A

Thyroid peroxidase - thyroiditis, hypothyroidism

Steroid 21-hydroxylase - adrenocortical failure (addison’s)

Glutamate decarboxylase (beta-cells of pancreatic islets) - autoimmune diabetes

23
Q

Name some intracellular molecules involved in transcription and translation

A

Double stranded DNA

Histones

Amino-acyl t-RNA synthases

Centromere proteins

24
Q

Genetic factors of autoimmune disease

A

Clusters within families

Alleles of MHC

25
Q

Which HLA allele is associated with diseases such as Sicca syndrome, Addison’s, Hashimoto thyroiditis and Myasthenia gravis disease?

A

DR3

26
Q

Environmental factors causing autoimmune disease

A

Infection - molecular mimicry, antigen breakdown and presentation changes, upregulation of co-stimulation

Drugs - molecular mimicry, genetic variation in drug metabolism

UV radiation - trigger for skin inflammation

27
Q

What is molecular mimicry

A

a structural similarity between self-proteins and microbial antigens that may trigger an autoimmune response

In systemic infection, the cross-reactivity will cause expansion of the responsive T-cell population recognising the self peptide

28
Q

Which microbial antigen is similar to a self antigen found in cardiac muscle which results in rheumatic fever

A

Group A streptococcal M protein

29
Q

Aim of treatment of autoimmune diseases (2)

A

Suppression of the damaging immune response - before irreversible damage to tissue, early detection is a challenge

Replacement of the function of the damaged organ - hypothyroidism, insulin dependent DM

30
Q

Type 1 diabetes mellitus cause

A

Juvenile onset

Destruction of pancreatic beta cells probably as a result of viral infection and genetic factors

Inadequate insulin secretion

31
Q

What are the 4 different types of pancreatic cells

A

Beta
Alpha
Delta
PP

32
Q

Aetiology of Type 1 Diabetes mention

A

Autoimmune destruction
- Circulatory antibodies to islet cells. Patients prone to develop other organ specific autoimmune diseases

Genetic factors

  • Association with certain HLA types
  • Environmental factors play a role too

Viral infection
- Antibodies to certain viruses are high in patients.
Viruses may act as triggers for autoimmune destruction e.g Coxsackie B or Mumps

33
Q

What can Hyperthyroidism result from? (6)

A 
Graves thyroiditis
Functioning adenoma
Toxic nodular goitre
Exogenous thyroid hormone (rare)
Ectopic secretion by ectopic thyroid tissue or tumours
34
Q

Grave’s thyroiditis

A

The most common cause of thyrotoxicosis.

Autoantibody (IgG) (LATS) which binds to thethyroidepithelial cells and mimics the action of TSH. LATS stimulates the function and growth ofthyroidfollicular epithelium.

It is an ‘organ specific’ autoimmune disease.

Usually associated with a diffuse goitre.

Increased vascularity.

35
Q

What is Cretinism

A

Caused by congenital thyroid deficiency

If hypothyroidism is present in the new-born, physical growth and mental development are impaired, sometimes irreversibly (cretinism).

Cretinism may be endemic in geographical areas where the diet contains insufficient iodine for thyroid hormone synthesis.

Sporadic cases are usually due to a congenital absence of thyroid tissue, or to enzyme defects blocking hormone synthesis.

36
Q

Hashimoto Thyroiditis

A

The most common cause of acquired hypothyroidism in adults.

In the early stages of Hashimoto thyroiditis, the damage to the thyroid follicles may lead to release of thyroglobulin causing a transient phase of thyrotoxicosis.

Hashimoto thyroiditis may initially cause thyroid enlargement, but later there may be atrophy and fibrosis.

37
Q

What do the 2 autoantibodies detectable in Hashimoto thyroiditis react with?

A

thyroid peroxidase

Thyroglobulin

38
Q

What are Autoimmune polyendocrine syndromes

A

A diverse group of clinical conditions characterised by functional impairment of multiple endocrine glands due to loss of immune tolerance.

Circulating autoantibodies and lymphocytic infiltration of the affected tissues or organs - eventually leads to organ failure.

The syndromes can occur in patients from early infancy to old age, and new components of a given syndrome can appear throughout life.

39
Q

Give examples of autoimmune polyendocrine syndromes

A

Frequently include conditions such as alopecia, vitiligo, celiac disease, and autoimmune gastritis with vitamin B12deficiency that affect nonendocrine organs.

40
Q

What is Autoimmune Polyendocrine Syndrome Type 1? what causes it?

A

Also named autoimmune polyendocrinopathy–candidiasis–ectodermal dystrophy is a rare autosomal recessive disease caused by mutations in the autoimmune regulator gene (AIRE).

41
Q

Clinical features of APS-1

A

At least two of three cardinal components during childhood:

Chronic mucocutaneous candidiasis

Hypoparathyroidism

Primary adrenal insufficiency (Addison’s disease)

Other typical features: enamel hypoplasia (teeth), Enteropathy with chronic diarrhea or constipation or primary ovarian insufficiency

42
Q

Autoimmune Polyendocrine Syndrome Type 2

A

Much more common than APS-1

Patients with APS-2 have at least 2 of the following endocrinopathies:
Type 1 diabetes
Autoimmune thyroid disease
Addison’s disease

The onset of APS-2 typically occurs in young adulthood, later than the onset of APS-1.

43
Q

X-Linked Immunodysregulation, Polyendocrinopathy, and Enteropathy (IPEX)

A

Extremely rare inherited syndrome

characterised by:
Early onset type 1 DM
Autoimmune enteropathy with diarrhoea and malabsorption
Dermatitis that may be eczematiform, ichthyosiform or psoriasiform

Eosinophilia and elevated IgE levels are frequently present in patients with IPEX.

Later manifestations of the syndrome may include:
Autoimmune thyroid disease
Alopecia
Various autoimmune cytopenias
Hepatitis
Exocrine pancreatitis.

Many features overlap with APS-1, but they usually develop much earlier in life than in APS-1.

44
Q

IPEX is frequently fatal in the first few years of life unless…

A

Patients are promptly treated with immunosuppressive agents or, if possible, with allogeneic bone marrow transplantation, which can cure the disease.

2ND YEAR SYSTEMS: Diabetes and Endocrinology (21 decks)

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