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Lecture

03 - January 22, 2013.docx

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Department
Immunology
Course
IMM250H1
Professor
All Professors
Semester
Winter

Description
PAPER PRESENTATION: B cells regulatory – one to five percent in system – expand when in contact with with CD19 – no B10 cells – used as negative control Monensin – to stain for intracellular cytokine production In vitro finding Cells increased three fold – IL10 in supernatant increased by five fold WHAT IS THE BIG PICTURE?? AUTOIMMUNE DISEASE Aberrant immune response from body – attack proteins expressed – result in pathology – can be fatal Chronic Pro-inflammatory environment – higher rate of diabetes type two, heart disease, etc. Striking sex difference – not all autoimmune diseases – systemic – females around nine or ten times more than males – strong female bias – Classification – organ specific or systemic (full blown; multiple organs affected) Type of immune response solicited in disease Examples of organ specific Trained to recognize certain antigen and that’s where the attack is oriented Type of immune effector mechanism in place – type of immune cells making attack on organ or myelin sheath – immune effector mechanism applicable broadly to immune responses in general Four diferent types of hypersensitivity – if already primed with antigen, and then exposed to same antigen, who cells involved in response to antigen? Classical allergy – mast cells – histamine release – inflammation in skin – no type one autoimmune diseases Type 2, 3, and 4 – main difference – in type 2 and 3, antibodies factor into major players of pathogenesis of these disorders – type 2 diseases, antibodies – Formation of immune complexes – antibodies are binding to things that form immune complexes, eliciting different type of immune response Type 4 – T cell that is main driver of pathology – multiple sclerosis – T helper cells are main driver of disease and initiation Type 2 – Graves disease – common cause of hyperthyroidism – Graves disease – autoantibody binding the thyroid stimulating hormone receptor – induces metabolism of thyroid hormone needed for body – autoantibody generated against THS receptor causing hyperactivation of receptor so more hyper thyroid Transfer to disease from mother to child – antibodies can cross into the fetus – M. Gravis – drooping eyelid – Antibodies have blocking function in disease – antibodies are specific against acetylcoline receptor – motor neurons – neuromuscular junction where they meet – into synaptic cleft – initiate muscles to contract – cuase unknown – autoimmune response initiated, block acetylcholine from binding and muscles cannot contract, people are weak Treatment of antibody disorders Short term – clean the blood – antibodies are effector molecules – filter out the antibodies – Long term – rituximab, B cell depleting agent – intravenous Ig pooled polyvalent IgG given every few months – polyclonal specificities Multiple sclerosis Neurons may die – cannot grow back Loss of neurons correlates with disability Lesions in the brain – Relapsing-remitting course – attacks of paralysis, sensational loss then get better; then recurrence of symptoms Spinal tap – sample of cerebral spinal fluid – run on gel – antibodies produced in cerebral spinal fluid, telling us some immune componenet to the disease Visualize brain of MS patient – lesions tend to occur in ventricles and mostly in brain; Gadolinium is a dye injected into the MS patient for MRI; if there is a leakage a blood brain barrier because of inflammation, dye can leak into brain and be visualized, to Two-phased disease Starts with relapsing remitting disease – gadolinium lesions in the brain, suggesting immune cells in the brain, attacking myelin Later on, brain atropy – brain is shrinking and losing neurons over time – chronic inflammatory process is inciting neurodegeneration – probably different than initial autoimmune attack Diagnosis criteria Active MS legion – myelin state is luxol fast blue – see when no blue means no myelin Blood vessels in the left photo – CD68 – macrophages in high numbers around blood vessels suggesting immune response cross into brain, perivascular location As immune response dies down at end of attack – area of lesion – in the middle of lesion, myelin not able to grow back – see edge of lesion, grey zone where there is evidence of some remyelation occurring – Sheaths that come back are thinner – may not be able to convey electrical signals as much Lesions in RRMS – lesions around ventricles; in secondary progression MS, areas of demyelination in the grey matter (where more neurons are) – suggesting initial myelin attack is spreading to other areas or other antigens Clusters of immune cells – boxed region – follicle-like structures where there are clusters of B cells, T cells dendritic cells – immune response has moved into CNS – lymph node like structures in the brain feeding continuing to feed the myelin destruction Gadolinium dye leaks into the No late disease – no longer have attack of peripheral immune cells into brain – do see immune system in the brain – detecting follicle structures in the brain, feeding destruction the brain – NOT SEEN IN MRI so do not see destruction of brain blood barrier so no enhancing legions No drugs for SPMS; multiple for RRMS – test drugs in EAE EAE Immunize w
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