Question 1 Please could you explain how lymphocytes (especially B) can maintain receptors on their surfaces? Is this genetically related? If so, when the lymphocytes are first exposed to the antigens, how could the antigen receptor be synthesized? Is there a mutation within the nuclei of these lymphocytes when they learn to make the receptors? If there is, can you explain how this occurs? Question 2 I understand how nuclear factor-κB (NFκB) works in the inflammatory response but what is the mechanism by which it causes cancer? Question 3 What are the diseases associated with hypocomplementaemia and which complement deficiency in particular? Question 4 What is meant by 'B lymphocytes are sensitive to clonal deletion'? Question 5 What are the immunological implications of 'bare lymphocyte syndrome'/MHC deficiency? Question 6 Please explain oligoclonal and monoclonal

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Question 1

Please could you explain how lymphocytes (especially B) can maintain

receptors on their surfaces? Is this genetically related? If so, when the

lymphocytes are first exposed to the antigens, how could the antigen

receptor be synthesized?

Is there a mutation within the nuclei of these lymphocytes when they

learn to make the receptors? If there is, can you explain how this occurs?

Question 2

I understand how nuclear factor-κB (NFκB) works in the inflammatory

response but what is the mechanism by which it causes cancer?

Question 3

What are the diseases associated with hypocomplementaemia and which

complement deficiency in particular?

Question 4

What is meant by 'B lymphocytes are sensitive to clonal deletion'?

Question 5

What are the immunological implications of 'bare lymphocyte

syndrome'/MHC deficiency?

Question 6

Please explain oligoclonal and monoclonal.

Question 7

I was wondering if there is any study regarding cell culture techniques of

CD4 helper cells (stem cell culturing) and, if so, is it of any benefit to

HIV-infected patients

Question 8

How do you define autoimmune disease?

Question 9

1. Why is dexamethasone not routinely used instead of prednisolone,

which is almost universally used routinely in autoimmune diseases, or

other indications for steroids? Is it because dexamethasone lacks the

mineralocorticoid activity seen with prednisolone and therefore does

not cause salt/water retention and hypertension?

2. Can high doses of dexamethasone be used in acute relapses of

multiple sclerosis (MS) in place of pulse methylprednisolone? If so,

what is the recommended dosage?

Question 10

What is meant by 'pus cell' and is this term synonymous with

neutrophils?