phoenix
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It's not surprising that some people have more than one since many have shared genetic associations.
There are quite a few studies that look at this.
This diagram shows pie charts for pairs of immune mediated diseases.
The green area represents shared genetic loci (ie places on the DNA where there are variations in the genetic 'code' that are known to carried by some of the people ( though not necessarily all) with the condition . )
The red colour represents loci that the are discordant ie variations that the other condition has but is not shared between the 2 diseases.
The size of the circle represents the number of known variants for the disease. (so inflammatory bowel disease has more known loci than psoriasis but a lot of this is down to the number of people tested in the various studies so the word known is important.)
The second diagram is called a Manhatten plot. It is the result of genome wide association studies(GWAS). This is where they look at many thousands of people's DNA matching the persons health conditions with small variations in the genetic code. They then analyse these variations to see if people with similar conditions share similar genetic variations.
The plot shows all the chromosomes in the genome and they are marked 1-22 plus the sex chromosomes along the bottom.. The columns show the loci ( places) where they have found DNA variants (SNPs) associated with the disease. The height of the columns show where there are higher numbers of these associations
ie It's the 'skyscrapers' that mark the places where gene variations seem to be linked to the condition.
As you can see quite clearly RA and T1 both have an area on chromosome 6 with many risk variants, Crohn's has a lesser number in this are but there are high associations on several other chromosomes..
Part of chromosome 6 contains genes of the HLA system that play an important part in the immune system coding for the proteins that should protect against bacteria and viruses. People are comparatively variable in this area and so we are quite diverse.
Also, we have one set of chromosomes from one parent and one set from the other so we have 2 chromosome 6s. In many cases a protective variation ( allele) from one parent may reduce or often counteract the effect of the allele from the other (so in LADA, it may be that we actually have some protective alleles that help prevent us from the fast onset classic T1 at a young age)
It's also important to realise that these condtions aren't 100% heritable there has to be something else that triggers the autoimmune reaction . Even if you are the identical twin (ie with identical genes) of someone with T1 , it is not certain you will develop it ; though in this case heritability may be as high as 88% ****.
Some of the conditions known to be related to variations of genes on chromosome 6
ankylosing spondylitis
Hashimotos (autoimmune) thyroiditis
Grave's Disease
Addinson's disease
narcolepsy (any one feel sleepy?)
psoriatic arthritis
RA
coeliac
Type 1 diabetes.
This site has lots of info about genes and conditions The link is to the HLA gene family but you can then go on to check the gene susceptibility for other conditions .
http://ghr.nlm.nih.gov/geneFamily/hla
Heritability estimates for various conditions.
http://www.snpedia.com/index.php/Heritability
*****
Not time to write about it but one possibility of a trigger (not the only one)are cells from a foetus that have crossed the placental barrier in pregnancy and vice versa. This I find quite fascinating, the idea that one has cells from ones children and mother remaining in the body. In one way I find it quite comforting but it is possible that the body may react against these 'foreign' cells.
There are papers that have found that women with thyroid problems often have these cells. Some researchers think that this particular trigger may be a reason for the fact that autoimmune disease as a whole (not T1) are more prevalent in women. There are lots of papers about other conditions and what is called microchimerism but I have only really looked at ones on the thyroid
The first link is to a New scientist article so explains it in non specialist terms
http://www.newscientist.com/article...m-siblings-aunts-and-uncles.html#.VBwIrJpBvIU
Fetal michrochimeric cells in autoimmune thyroid disease, harmful, beneficial or innocent for the thyroid gland?
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3921191/
(answer we don't know but it may well depend on your HLA haplotype (ie the variations in the HLA system of the genome ie chromosome 6)
(now back to my real genetics course, I've just wasted a long time because although the whole genetics thing fascinates me, it's really hard to explain in layperson terms )
There are quite a few studies that look at this.
This diagram shows pie charts for pairs of immune mediated diseases.
The green area represents shared genetic loci (ie places on the DNA where there are variations in the genetic 'code' that are known to carried by some of the people ( though not necessarily all) with the condition . )
The red colour represents loci that the are discordant ie variations that the other condition has but is not shared between the 2 diseases.
The size of the circle represents the number of known variants for the disease. (so inflammatory bowel disease has more known loci than psoriasis but a lot of this is down to the number of people tested in the various studies so the word known is important.)
The second diagram is called a Manhatten plot. It is the result of genome wide association studies(GWAS). This is where they look at many thousands of people's DNA matching the persons health conditions with small variations in the genetic code. They then analyse these variations to see if people with similar conditions share similar genetic variations.
The plot shows all the chromosomes in the genome and they are marked 1-22 plus the sex chromosomes along the bottom.. The columns show the loci ( places) where they have found DNA variants (SNPs) associated with the disease. The height of the columns show where there are higher numbers of these associations
ie It's the 'skyscrapers' that mark the places where gene variations seem to be linked to the condition.
As you can see quite clearly RA and T1 both have an area on chromosome 6 with many risk variants, Crohn's has a lesser number in this are but there are high associations on several other chromosomes..
Part of chromosome 6 contains genes of the HLA system that play an important part in the immune system coding for the proteins that should protect against bacteria and viruses. People are comparatively variable in this area and so we are quite diverse.
Also, we have one set of chromosomes from one parent and one set from the other so we have 2 chromosome 6s. In many cases a protective variation ( allele) from one parent may reduce or often counteract the effect of the allele from the other (so in LADA, it may be that we actually have some protective alleles that help prevent us from the fast onset classic T1 at a young age)
It's also important to realise that these condtions aren't 100% heritable there has to be something else that triggers the autoimmune reaction . Even if you are the identical twin (ie with identical genes) of someone with T1 , it is not certain you will develop it ; though in this case heritability may be as high as 88% ****.
Some of the conditions known to be related to variations of genes on chromosome 6
ankylosing spondylitis
Hashimotos (autoimmune) thyroiditis
Grave's Disease
Addinson's disease
narcolepsy (any one feel sleepy?)
psoriatic arthritis
RA
coeliac
Type 1 diabetes.
This site has lots of info about genes and conditions The link is to the HLA gene family but you can then go on to check the gene susceptibility for other conditions .
http://ghr.nlm.nih.gov/geneFamily/hla
Heritability estimates for various conditions.
http://www.snpedia.com/index.php/Heritability
*****
Not time to write about it but one possibility of a trigger (not the only one)are cells from a foetus that have crossed the placental barrier in pregnancy and vice versa. This I find quite fascinating, the idea that one has cells from ones children and mother remaining in the body. In one way I find it quite comforting but it is possible that the body may react against these 'foreign' cells.
There are papers that have found that women with thyroid problems often have these cells. Some researchers think that this particular trigger may be a reason for the fact that autoimmune disease as a whole (not T1) are more prevalent in women. There are lots of papers about other conditions and what is called microchimerism but I have only really looked at ones on the thyroid
The first link is to a New scientist article so explains it in non specialist terms
http://www.newscientist.com/article...m-siblings-aunts-and-uncles.html#.VBwIrJpBvIU
Fetal michrochimeric cells in autoimmune thyroid disease, harmful, beneficial or innocent for the thyroid gland?
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3921191/
(answer we don't know but it may well depend on your HLA haplotype (ie the variations in the HLA system of the genome ie chromosome 6)
(now back to my real genetics course, I've just wasted a long time because although the whole genetics thing fascinates me, it's really hard to explain in layperson terms )
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