#autoimmunity

[thelupuslady]

[longhaulerbear]

Several of the most prevalent new-onset autoantibodies have, to our knowledge, not been described previously, including the three with the highest prevalence, i.e., anti-CCDC63 (coiled-coil domain-containing protein 63), anti-TRIM63 (E3 ubiquitin-protein ligase TRIM63), and anti-SNURF (SNRPN upstream reading frame protein)

[lasseling]

Covid mRNA ‘Vaccines’ Trigger Multiple Sclerosis, Study Finds

A team of investigative medical researchers has found that Covid mRNA “vaccines” are responsible for several new cases of multiple sclerosis.

[science-sculpt]

The T Cell Landscape

T cells, a critical component of the adaptive immune system, stand as the body's elite force in combatting infections and diseases. These specialized lymphocytes boast remarkable diversity, each type playing a distinct role in orchestrating a targeted and effective immune response.

T cells, like all blood cells, originate from hematopoietic stem cells residing in the bone marrow. However, their training ground lies within the thymus, a specialized organ located in the chest. Here, they undergo a rigorous selection process known as thymocyte education. During this process, immature T cells, called thymocytes, are presented with self-antigens (molecules unique to the body) by special cells. Thymocytes that bind too strongly to these self-antigens are eliminated, preventing them from attacking healthy tissues later. Only thymocytes that demonstrate the ability to recognize foreign invaders while exhibiting tolerance to self are released into the bloodstream as mature T cells.

Following this rigorous training, mature T cells exit the thymus and embark on their patrol, circulating throughout the bloodstream and lymphatic system. They remain vigilant, constantly scanning for their specific targets – antigens. Antigens are foreign molecules, such as fragments of viruses, bacteria, or even cancerous cells, that trigger the immune response.

The hallmark of a T cell is its T cell receptor (TCR), a highly specialized protein complex embedded on its surface. This receptor acts like a lock, uniquely shaped to fit a specific antigen, the "key." Each T cell develops a unique TCR capable of recognizing only a single antigen, enabling a highly specific immune response.

But how do T cells encounter these hidden antigens lurking within infected or cancerous cells? This critical role is played by antigen-presenting cells (APCs). APCs, such as macrophages and dendritic cells, engulf pathogens or abnormal cells, break them down into smaller fragments (peptides), and present them on their surface complexed with major histocompatibility complex (MHC) molecules. MHC molecules act as identification tags, allowing T cells to distinguish between "self" and "non-self." When a T cell's TCR encounters its specific antigen bound to an MHC molecule on an APC, a dance of activation begins. The T cell becomes stimulated, and a cascade of signaling events is triggered. This leads to the T cell's proliferation, producing an army of clones specifically tailored to combat the recognized threat.

T cells are not a single, monolithic entity. They comprise a diverse population, each type with a specialized function:

Helper T Cells (Th Cells):

Helper T cells, often abbreviated as Th cells, play a central role in coordinating immune responses. They express the CD4 surface marker and can recognize antigens presented by major histocompatibility complex class II (MHC-II) molecules. Subtypes of helper T cells include Th1, Th2, Th17, and regulatory T cells (Tregs), each with distinct functions and cytokine profiles.

Th1 cells mediate cellular immunity by activating macrophages and cytotoxic T cells, crucial for defense against intracellular pathogens.

Th2 cells are involved in humoral immunity, promoting B cell activation and antibody production, thus aiding in defense against extracellular parasites.

Th17 cells contribute to the immune response against extracellular bacteria and fungi, producing pro-inflammatory cytokines. Regulatory T cells (Tregs) maintain immune tolerance and prevent autoimmunity by suppressing excessive immune responses.

Cytotoxic T Cells (Tc Cells):

Cytotoxic T cells, also known as Tc cells or CD8+ T cells, are effector cells responsible for directly killing infected or aberrant cells. They recognize antigens presented by MHC class I molecules on the surface of target cells. Upon activation, cytotoxic T cells release perforin and granzymes, inducing apoptosis in target cells and eliminating the threat.

Memory T Cells:

Memory T cells are a long-lived subset of T cells that persist after the clearance of an infection. They provide rapid and enhanced immune responses upon re-exposure to the same antigen, conferring immunological memory. Memory T cells can be either central memory T cells (TCM), residing in lymphoid organs, or effector memory T cells (TEM), circulating in peripheral tissues.

γδ T Cells:

Unlike conventional αβ T cells, γδ T cells express a distinct T cell receptor (TCR) composed of γ and δ chains. They recognize non-peptide antigens, such as lipids and metabolites, and are involved in immune surveillance at epithelial barriers and responses to stress signals.

Beyond the Battlefield: The Expanding Roles of T Cells: The remarkable capabilities of T cells have opened doors for several groundbreaking applications in medicine:

Vaccines: By presenting weakened or inactivated forms of pathogens, vaccines "train" the immune system to generate memory T cells. This prepares the body to recognize and rapidly eliminate the real pathogen upon future exposure, preventing disease.

Cancer immunotherapy: CAR T-cell therapy, a revolutionary approach, genetically engineers a patient's own T cells to express chimeric antigen receptors (CARs) that recognize and target specific cancer cells. These "supercharged" T cells are then reintroduced into the patient, unleashing a potent attack against the tumor.

Autoimmune disease treatment: Researchers are exploring ways to manipulate T cells to suppress harmful immune responses that underlie autoimmune diseases like rheumatoid arthritis and multiple sclerosis.

The diverse array of T cells underscores the immune system's complexity and adaptability in mounting tailored responses against a myriad of threats. From orchestrating immune reactions to maintaining tolerance and establishing long-term immunity, T cells play multifaceted roles in safeguarding the body's health. Understanding the intricacies of T cell biology not only sheds light on immune-mediated diseases but also paves the way for developing novel therapeutic strategies harnessing the power of the immune system.

T cells represent a fascinating aspect of immunology, with their diversity and specificity driving the complexity of immune responses. As research advances, further insights into T cell biology promise to revolutionize immunotherapy and enhance our ability to combat diseases ranging from infections to cancer. By understanding and harnessing their power, we can unlock new avenues for protecting and improving human health.

[the-diabolic-acid]

[severeprincesheep]

Mikhaila Peterson Reports Back After 5 Years on Carnivore Diet

[disabledsysboxes]

Autoimmune - 6

[gancanagh]

...Some people know me as hope...

So cower at the man I've become when I sing from the top of my lungs

That I won't retire, I'll stand in your fire, inspire the meek to be strong

And when I am gone, I will rise in the music that I left behind

Ferocious, persistent, immortal like you, we’re a coin with two different sides

[what-remains-of-wren]

I think what people underestimate most about chronic and repeated childhood trauma is that it truly effects every single proportion of you.

There is some theory at the moment that a component of depression is inflammation. This isn’t just out of left field, since clinical encephalitis is well demonstrated to cause psychosis. Encephalitis is inflammation of the brain and it causes neuropsychiatric symptoms like you have never seen before- and is usually quite hard to detect on labs until someone starts having siezures- by which point you’re in shit.

This is partly why fibromyalgia symptoms are treated with antidepressants, and why depression can have some wicked somatic symptoms- they’re not two seperate things- treat the body to treat the brain, or if the brain is convinced the body is being hurt because you feel some sort of pain all the time- emotional or psychological- treat the brain.

It’s not as simple as one thing causing the other either. Inflammation is a mistaken immune response. One of the major effects of cortisol, the hormone released when you are chronically stressed, is that you stop producing things you don’t need to produce. Processes stop working where they should and can even affect your immune system. Recurrent trauma stops your body from producing it’s own natural inflammatories.

Stress also causes epigenetic changes. These are heritable. These can mute and activate genes- most notably those responsible for stopping cancer. It is possible for your mother or father to have a stressful period in life, epigenetic changes to happen, and then for you to be born with those already happening. 

The majority of autoimmune conditions have stress- acute or chronic- as a major trigger factor. Stress isn’t just in the head. You produce hormones, you make protiens, you make antibodies- sometimes ones you shouldn’t. Mental and physical health aren’t too seperate, especially not when it comes to this area.

 What I’m saying is that what you’ve gone through isn’t just in your head. Chances are it’s in your body as well. So don’t expect to just feel it in your head.

[nicolagriffith]

Snippets—Women and autoimmune disease, the first wine, early Americans, and how cats purr

For Sunday: snippets of science news on some of my favourite things in life (well, the favourite things we can talk about in polite company): cats, wine, and humans in the Americas, plus one of my ongoing personal concerns, autoimmune disease. Some weight

Some of this stuff dates from late last year when I was too busy with Menewood stuff to comment. But as some of my favourite things in life (well, the favourite things we can talk about in polite company) are cats, wine, and history, and as one of my ongoing personal concerns is autoimmune disease, I thought, Eh, let’s combine them. We’ll start with the weighty stuff first then lighten up a…

[ghostzussy]

"Why are you wearing a mask again why are you afraid" BECAUSE I'M AUTOIMMUNE AND MY IMMUNE SYSTEM CAN'T TAKE ANOTHER L PLS

[thelupuslady]

[longhaulerbear]

The paper presents a systematic review assessing the role of autoimmunity in ME/CFS, specifically focusing on the association of autoantibodies and immune dysregulation with the condition's pathogenesis.

Findings from the review suggest insufficient evidence to classify ME/CFS as an autoimmune disease due to the absence of specific autoreactivity and tissue damage typically seen in autoimmune conditions.

Notable studies within the review explore cytokine signaling, genetic factors, and the prevalence of autoantibodies, with mixed results that highlight the complexity of ME/CFS.

Future research is vital for developing diagnostic and treatment strategies that accurately address the multifactorial nature of ME/CFS, especially as the post-COVID-19 landscape may increase its prevalence.

The evidence as a collective, suggests that immune dysregulation and the presence of AAb in people with ME/CFS may play a role in the contribution to specific symptoms or comorbidities. However, there is a lack of evidence to suggest ME/CFS is an autoimmune condition. It is critical to recognise the broader and more specific limitations of these studies, such as that of small sample sizes and the need for further mechanistic research to establish causal relationships and clinical significance. Notably, the heterogeneity of AAb profiles amongst ME/CFS patients underscores the complexity of this phenomenon and highlights the necessity for personalised approached to diagnosis and treatment.

Whilst there exists evidence suggestive of immune deregulatory phenomena and autoantibodies in ME/CFS patients, these findings cannot deduce ME/CFS to an autoimmune disease. These findings underscore the pressing need for further research to unravel the precise immunological and genetic factors at play in ME/CFS. With direct emphasis on distinguishing autoimmunity from broader immune dysregulation, such targeted efforts will ultimately pave the way for more effective diagnostic and therapeutic strategies in the ongoing quest to understand and manage this enigmatic condition.

[the-archenlandian-court]

Me: *wiping sweat off myself because I’m allergic to it*

It is 33*c today 😭

[caffeine-and-sunshine]

We don’t post about this a lot and my host is the primary symptom holder for the body’s disabilities. But it IS disability pride month.

We have EDS, a genetic and progressive connective tissue disorder. This illness is infamous for causing daily dislocated and subluxated (partially dislocated) joints. People think we exaggerate when we do all kinds of weird moves to put our joints back in. We’ve been told countless times that it’s “not possible” for ribs to slip out of place.

We also have a host of autoimmune issues that attack and damage (often permanently) my joints.

Put together, they’ve created two new diagnoses just on their own.

1. Slipping rib syndrome, where my ribs NEVER stay in place and will require extensive back surgery to use metal to plate my ribs to where they are supposed to be so that they cannot slip anymore.

2. Moderate to severe Osteoarthritis in our back (due to the ribs), fingers, hips and knees. Keep in mind the body is only 29. Keep in mind these are just a FEW examples from our novel-length diagnosis list.

It’s never JUST cancer. It’s never JUST lupus or JUST autonomic function. There is ALWAYS more going on. Be kind! Be patient! Assume the best in people, ESPECIALLY disabled people. We’re not being lazy. We just had to re-learn how to live and get things done to work around the things we can no longer do.

i would like to remind everyone that most disabilities come with comorbidities. what this means is that, most of the time, someone who is disabled does not have just *one* condition that causes them pain or difficulty.

for example, i have crohn's, which is an autoimmune disease primarily affecting the bowels. i also have ehlers-danlos syndrome(eds), which is a connective tissue disorder. eds can make crohn's worse because eds can affect your intestinal lining. crohn's can make eds worse because crohn's can also affect joint inflammation, so loose joints become more inflamed than they otherwise would. both can severely affect fatigue levels.

these are just two things i deal with. there are other comorbidities and complications i deal with, like fibromyalgia, dysautonomia, nerve damage, and more; but eds and crohn's are the easiest to explain how they play off each other.

i don't think abled people realize that most disabled people deal with something like this. i see disabled people online being very open about their multiple diagnoses to raise awareness and understanding - and then i see abled people shitting on them because "there's no way you can have that many things wrong with you."

but this is the truth of the situation: being disabled is almost never a straightforward, one-and-done diagnosis thing. even if it starts as one diagnosis, many people discover or develop other problems as their health changes. or even develop other issues because of medications! the intravenous medication i took for crohn's causes arthritis in a significant number of patients, and is most likely responsible for just how severe my joint inflammation gets.

so if you're abled, and you've ever seen a long diagnosis list and thought maybe someone was exaggerating - please step back and rethink. this is a very common thing. i would dare to guess that more people are multi-diagnosis than single-diagnosis. you are not helping anyone by accusing someone of faking or exaggerating, you are just being ableist.

as a disabled person, it takes immense bravery to speak openly and publicly about how our lives are affected by our disabilities, and we do not deserve to be treated poorly for being honest about our realities. your lack of knowledge or willingness to learn should not become our additional pain.