Couple of questions for immunity:
Would I be correct in saying dendritic cells process antigenic material and display their antigens on their MHC 2 markers for T helper cells to recognise, thus providing a link to the adaptive immune response. Is it specifically targeting T helper cells or other leukocytes as well?
This is good! Although I would specify that dendritic cells present pathogenic/non self antigens on the mhc class 2 receptors. Realistically dendritic cells do present not just pathogenic antigens, but as far as our course is concerned, dendritic cells just present pathogenic antigens.
Realistically dendritic cells will bind to other cells like cytotoxic T cells and what not, but these specifics aren't relevant to the course. Just know that they bind to the t helper cell as you have mentioned.
Am I right in saying MHC 1 markers displays antigens produced by the presenting cell whereas MHC 2 markers displays nonself antigens outside the presenting cell?
Yes. This sounds right!
How would one describe how a person produces more antibodies during secondary exposure to specific antigen than the first exposure (basically how would I explain memory B cells and how they develop immunological memory - just looking for a more concise explanation than the one I have)
As a result of a primary immune response, memory b cells specific to the antigen illiciting this response are produced. These memory b cells exist in a greater number relative to that of the nieve cells in a primary infection such that secondary infections are characterised by a faster and greater antibody production.
Basically, because of memory b cells, there are more cells that can potentially bind to the antigen and be activated by t helper cells such that the immune response occurs faster and to a greater extent.
Does this help?
How specifically does inflammation response benefit the immune response? Do I just need to say it attracts phagocytes and large molecules to site of infection helping develop a rapid innate response via physiological changes.
The inflammation response involves many different aspects which all contribute to the immune response. It's not just the case that inflammation involves the release of cytokines which attract other immune cells to the region of infection, but this is certainly one major part of the inflammation response. You could use that as an answer. You could also talk about the vasodilation and adaptations to the local vasculature that enable the migration of immune cells.
MHC 1 and 2 markers are all proteins, all antibodies are proteins, not all antigens are proteins, all MHC 2 markers are made of antibodies - is my understanding correct?
This is correct except mhc class 2 receptors are not antibodies. You might be thinking about b cell receptors which are surface bound antibodies.
Why would a vaccine that contains the pathogen in an inactivated form be less effective than one where it is in an weakened form? I'd assume because since its dead it elicits a weaker adaptive immune response and weaker immunological memory but need someone to expand on this please
Not entirely sure about this, but your reasoning seems quite sound. Remember that an immune response is illicited by the sensing of damage and/or danger from the immune system. If the virus is completely inactive it won't cause damage and thus has a much lower chance of Illiciting an immune response
In multiple sclerosis, the B and T cells are involved in targeting the myelin sheathe of neurons as a result of failure of self-tolerance. Is it also due to mitochondria in oligodendrocytes breaking down that leads to destruction of myelin sheathe? If the second part is true do I have to mention this?(just feels like its out of the study design and not required)
You are right. This is out of the study design and you do not need to know this.
How much do we need to know about types of pathogens such as prions and worms, I know their names but what features should I know about them?
You don't need to know much. This content is usually examined through questions asking you to simply identify the pathogen from basic characteristics. So just know the key features of each one. You don't need the specifics of how they function. Hobestly worms, virions, prions and fungi are not all That prevelant, atleast from my own experience. The main thing is understanding and being able to differentiate between viruses and bacteria.
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Are T helper cells activated by antigen presenting cells specifically macrophages and dendritic cells or can they be activated by cells that display nonself antigens on their MHC 1 markers?
Thanks in advance 
Must be by mhc class 2 markers, thus must be by a macrophage or dendritic cell.
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