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Question: SIR,I was reading 1st chapter of kuby and I am not getting the meaning of this line i.e."serum from an animal inoculated with non infectious material would nevertheless react with the injected material in a specific manner"? Can u please explain ???
By: tania banerjee     Date: 2012-08-04

Answer: We are living in world filled with microbes, therefore, there will be "natural antibodies" that are produced to commensal microbes etc. Therefore, it is likely that there are some antibodies that cross-react with non-infectious (e.g.commensal) and infectious (e.g. pathogens) materials.

By: Dr. Dipankar Nandi     Email: tanyangel32@gmail.com     Date: 2012-09-08


Question: thank u so much sir
By: tania banerjee     Date: 2012-09-15

Answer: You are welcome!

By: Prof. Anjali Karande     Email: tanyangel32@gmail.com     Date: 2012-10-01


Question: Wat is difference between chimeric and humanised antibodies? Even humanised antibody molecules have a murine portion.... Wat is the criteria to call an antibody humanised?
By: Dr P Krishnadas     Date: 2012-10-16

Answer: Humanised antibodies are antibodies of non-human origin but their constant domains are replaced by human constant domain sequences so as to nullify immunogenicity. Chimeric antibodies on the other hand are simply 'hybrid antibody molecules' which could even be a dimer of two different antigen-binding heavy and light chains (for eg., those designed for use in immunohistochemistry). In other words, a humanised antibody called a chimera but a chimera need not be a humanised antibody.

By: Prof. Anjali Karande     Email: krishnadaspnair@gmail.com     Date: 2012-10-22


Question: Thanks for explaining the concepts sir. The question was from immunopharmacology perspective where suffix -mumab is used for murine antibodies -ximab for (so called)chimeric antibodies and -zumab for humanised antibodies. Is there a difference in synthesis of -ximab and -zumab?
By: Dr P Krishnadas     Date: 2013-02-12

Answer: These are suffixes and prefixes that are used to refer to pharmacological 'drugs' or medicines in the market. International conventions or societies decide on these although many of these as I read them are a little confusing. Your question is a difficult one and cannot be addressed by a simple description. Please refer to a couple of web sites -- I am giving two of them that I found here for helping you understand (http://en.wikipedia.org/wiki/Nomenclature_of_monoclonal_antibodies and http://en.wiktionary.org/wiki/-mab). So far as synthesising them -- as far as my knowledge goes, they have to be done using rDNA cloning and expression since they use sequences from different animal antibodies. These cloned genes are then overexpressed in various systems to produce the desired protein. No single animal can be made to produce them such as in the case of immunisation of rabbit/mouse/etc with an antigen.

By: Dr. R. Manjunath     Email: krishnadaspnair@gmail.com     Date: 2013-02-22


Question: sir/madam,as we know thousands of B-cells and T-cells are produced with each having different antigenic or MHC specificity.Thus, it may be possible to have ,within these, cells that are recognizing \'self\' as \'non-self\' and mounting immune response.So,how does body tackle the problem and filter them?
By: Anubhav     Date: 2013-10-04

Answer: This is a good question, Anubhav - it has intriqued several generations of immunologists. I am happy that you asked this question. It is true that the body generates several millions of B cell receptors and T cell receptors with the hope that some them will bind to a cognate antigen and protect the host. A problem is that some of these receptors may bind host proteins. The majority of BCRs and TCRs that recognize self are deleted during the maturation of B cells (in fetal liver and bone marrow) and T cells (in thymus). Thus, the B cells and T cells in the periphery are ones that do not see self. Now this is not fool proof as in some cases (minority) autoimmunity occurs. However, for the majority this works well.

By: Dr. Dipankar Nandi     Email: anubhavkaphle@gmail.com     Date: 2013-10-11


Question: sir/madam,as we know thousands of B-cells and T-cells are produced with each having different antigenic or MHC specificity.Thus, it may be possible to have ,within these, cells that are recognizing \'self\' as \'non-self\' and mounting immune response.So,how does body tackle the problem and filter them?
By: Anubhav     Date: 2013-10-04

Answer: This is a good question, Anubhav - it has intriqued several generations of immunologists. I am happy that you asked this question. It is true that the body generates several millions of B cell receptors and T cell receptors with the hope that some them will bind to a cognate antigen and protect the host. A problem is that some of these receptors may bind host proteins. The majority of BCRs and TCRs that recognize self are deleted during the maturation of B cells (in fetal liver and bone marrow) and T cells (in thymus). Thus, the B cells and T cells in the periphery are ones that do not see self. Now this is not fool proof as in some cases (minority) autoimmunity occurs. However, for the majority this works well. In addition, recent discovery of a new autoimmune disease in humans called the APS-1 syndrome shows that a gene called AIRE is responsible for expression of many self antigens in the thymus which are seen by T cells and those that recognise these with very high avidity are deleted -- remember that the TCR recombination occurs before these events and the TCR is needed for the recognition of self antigens in the thymus. Mice knocked out for AIRE suffer from self antibodies to many endocrine organs and retina. Only those T cells that recognise with intermediate affinity are allowed to proliferate and go into the periphery. Those that do not recognise or recognise self antigens with low affinity with low affinity will not get the signal to proliferate and hence die. Despite these processes, there are T cells that go into the periphery that can recognise self but are kept in check by various mechanisms. This tolerance can break down when that T cells sees an antigen that is crossreactive to self and then autoimmunity can be triggered. So it is as mentioned above a complex process.

By: Dr. R. Manjunath     Email: anubhavkaphle@gmail.com     Date: 2013-10-11


Question: Thank u sir for the explanation.
By: Anubhav     Date: 2013-10-20

Answer: You are welcome!

By: Dr. Dipankar Nandi     Email: anubhavkaphle@gmail.com     Date: 2013-11-01


Question: Could you please let me know the difference between antigen and pathogen.Suggest some references .In most of the cases both are being used as synonymous to each other Thanking you sir
By: sreeram     Date: 2013-11-13

Answer: A pathogen is anything that can cause a disease, eg., bacteria, viruses etc. An antigen is defined as molecules that can bind to the product of an immune response eg., antibodies produced by B cells. Pathogens have antigens and several of them in one pathogen.

By: Prof. Anjali Karande     Email: sreeramtlpd@gmail.com     Date: 2013-11-25


Question: Sir/madam during the processing of antigens by Dendritic cells or any APC\'s , the proteins are broken down into fragments.I am confused about which fragments will bind to MHC-II. Does it depend on the variable region in the groove of a1 b1 domain or any other things?
By: Anubhav     Date: 2013-12-22

Answer: The binding of peptides generated in the MIIC (MHC class II compartments) compartments depends on several factors. Basically peptides that bind to the correct MHC class II allele will be strongly selected for binding, e.g. anchor residues, ability to be cleaved by Cathepsins etc. Remember the DM molecules plays the role of Editor to ensure that high affinity peptides bind MHC class II. In the absence of DM, most MHC class II are bound by CLIP which is a peptide derived from Invariant chain.

By: Dr. Dipankar Nandi     Email: anubhavkaphle@gmail.com     Date: 2014-01-04
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