Download presentation
Presentation is loading. Please wait.
1
Clinical Immunology Jasmina Makarevic
ATTA-UR-RAHMAN SCHOOL OF APPLIED BIOSCIENCES (ASAB) Clinical Immunology Jasmina Makarevic Fall Semester 2016
2
Autoimmune diseases Jasmina Makarevic
3
The autoimmune diseases we looked at until now….
Haematological diseases: Haemalytica anermias Warm haemolytic anaemias Cold haemaolytic anaemias Joints and Muscels: Rheumatoid arthritis Chronic arthritis Systemic lupus erythematosus Thyroid diseases: Hashimoto thyroiditis Graeves disease Pancreas: Diabetes mellitis: Typ1 and Typ 2 Jasmina Makarevic
4
Neuroimmunology Normal:
The immune system participate actively in nervous tissue to counteract infection- Cells which enter these tissues in inflammation (T and B lymphocytes as well as macrophages) Autoimmune Disease: Damaging the own neuronal system! Which diseases we will look at: Multiple scelorosis Mystenia gravis Jasmina Makarevic
5
Multiple sclerosis (MS)
Demyelining diseases of the central nervous system The insulating covers of nerve cells in the brain and spinal cord are damaged. It is an inflammatory disease of white matter in the central nerval system This damage disrupts the ability of parts of the nervous system to communicate, resulting in a wide range of signs and symptoms. MS is common in Caucasians (1 case per 2000) It is a hugely variable disease in term of progress, disability… Clinical diagnosis can be difficult; clinical features depend on the site of the pathological lesion in the brain. Many plaques are clinical silent! The rate of new lesionsis unpredictable and also variable It depends on the recovery between the attacks Jasmina Makarevic
6
How to diognose? The patological lesion in MS, is a ‚plaque‘: this is an area of the white matter in which myelin and oligodendrocytes are absent. Myelin is a protein-phospholipid material that surrounds axons in a multilayered, dense spiral. Myelin sheats in the CNS are formed by compacted membranes of oligodentrocyte function Axons without myelin sheats are poor conductors of nerve impulse. Jasmina Makarevic
7
Immunopathogenesis of demyelination
In the early stage of the plaque there is an oedema, apoptopic oligodentrocytes and infiltrating cells. (B- cells are involved in the local production of Ig, whilst T-cells and macrophages are involved in the acute Inflammotory process) Jasmina Makarevic
8
At a glance: Symptoms of Mutiple Sclerosis
Jasmina Makarevic
9
Progression of MS Jasmina Makarevic
10
Mystenia gravis Autoimmune diseases of the neuromuscular junction
It is un uncommon disease Characterized by weekness and fatigues of voluntary muscels, including those of the eys. The weekness results from impaired transmission from nerv to muscle at the neuromuscular junctions. Neurotransmission is impaired by autoantibodies to the acetylincholine receptores in the postsynaptic membrane of the muscle These antiodies reduce the number of receptors: Complement-mediated lysis and Accelerated internalization Blocking the receptors Jasmina Makarevic
11
How does it function? Jasmina Makarevic
12
Symptoms at a glance Jasmina Makarevic
13
Ptosis (drooping of the eyelid)
Jasmina Makarevic
14
Evidence that Myasthenia Gravis is an Autoimmune disease
Strong associateion with organ-specific autoimmune diseases such as diabetes, in an individual patient Increased incidence of organ-specific autoimmune diseases in close family members Thymic abnormalities, including B-cell forming follicles Occurence of a transient form of MG in 10% of newborn babies of myastenic mothers Jasmina Makarevic
15
Immunodeficiency Primary: They may involve adaptive or
Immune response and may be permanante (genetic) ot transiente (due to viral infection) Jasmina Makarevic
16
Defects in immunity Jasmina Makarevic
17
Primary Antibody deficiencies
Jasmina Makarevic
18
Types of Primery deficiencies
Jasmina Makarevic
19
B-cell maturation Jasmina Makarevic
20
Outlook Deeper look into Immunodeficiency diseases Primary Secondary
Jasmina Makarevic
21
Thank You for Your Attention!
Jasmina Makarevic
Similar presentations
© 2025 SlidePlayer.com. Inc.
All rights reserved.