Stories about: immunology

News Note: Steroids could be counter-productive in severe asthma

severe asthma
Nine years old kid with allergic asthma, inhaling his medication through spacer while looking at with his wide opened eyes perhaps he is getting energy boost

Some 10 to 15 percent of people with asthma have severe disease that medications can’t control. A deep-dive multicenter study finds differences in these patients’ immune systems that may explain why increased dosages of corticosteroids don’t help — and could lead to steroids doing more harm than good. Findings appear online this week in Science Immunology.

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Poison ivy and psoriasis: The treatment we’ve been itching for?

poison ivy psoriasis target CD1a
Poison ivy, psoriasis, eczema and other inflammatory skin conditions could have a shared targeted treatment. (Jessica Kim/Winau Lab)

The skin is a natural barrier against pathogens and harmful chemicals. But it isn’t bulletproof: contact allergens like poison ivy can trigger an immune response causing severe inflammation, itching and tissue damage. Mechanistically, what happens is that Langerhans cells — certain antigen-presenting cells in the immune system — initiate a chain reaction. This rallies helper T cells to the area, causing skin inflammation.

A protein called CD1a (Cluster of Differentiation 1a) has been thought to be part of this reaction. But until recently, its role was poorly understood, at least in part because there was no good test model. Research in Nature Immunology now suggests that targeting CD1a could lead to new therapies for poison ivy and other inflammatory skin conditions like psoriasis and eczema.

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Protecting immune cells from exhaustion

T cell exhaustion
Boosting a naturally occurring protein could prevent T-cells from burning out

Run the first half of a marathon as fast as you can and you’ll likely never finish the race. Run an engine at top speed for too long and you’ll burn it out.

The same principle seems to apply to our T cells, which power the immune system’s battle with chronic infections like HIV and hepatitis B, as well as cancer. Too often, they succumb to “T cell exhaustion” and lose their capacity to attack infected or malignant cells. But could T cells learn to pace themselves and run the full marathon?

That’s the thinking behind a research study published last week by The Journal of Experimental Medicine. “Our research provides a clear explanation for why T cells lose their fighting ability,” says Florian Winau, MD, “and describes the countervailing process that protects their effectiveness.”

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When antibiotics fail: A potential new angle on severe bacterial infection and sepsis

bacterial infection sepsisBacterial infections that don’t respond to antibiotics are of rising concern. And so is sepsis — the immune system’s last-ditch, failed attack on infection that ends up being lethal itself. Sepsis is the largest killer of newborns and children worldwide and, in the U.S. alone, kills a quarter of a million people each year. Like antibiotic-resistant infections, it has no good treatment.

Reporting this week in Nature, scientists in Boston Children’s Hospital’s Program in Cellular and Molecular Medicine (PCMM) describe new potential avenues for controlling both sepsis and the runaway bacterial infections that provoke it.

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Can we supercharge vaccines? Added compound boosts T-cell production

supercharged vaccines oxPAPCBridging our innate and adaptive immune systems, dendritic cells are sentinels that circulate in the body searching out microbes and activating T-cells to destroy the invaders. They do this by presenting bits of the microbes on their surface—explaining why they’re often called antigen-presenting cells.

Reporting in Science this week, researchers describe a way to push dendritic cells into a “hyperactive” state, supercharging their ability to rally T-cells.

The key player, a fatty chemical called oxPAPC, is naturally found in damaged tissues and atherosclerotic plaques. It selectively targets dendritic cells and could, the researchers believe, enhance people’s immunity to a wide range of infections.

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Food allergies: Turning tolerance back on

Mast cell food allergy
Mast cells don’t simply cause acute allergic reactions. They also turn off immune tolerance. But that could change. (Bruce Blaus/Wikimedia Commons)

Hans Oettgen, MD, PhD, is Associate Chief of the Division of Allergy and Immunology at Boston Children’s Hospital.  He leads a research group investigating mechanisms of allergic diseases.

Not long ago I received a wonderful email from “Sam,” an 18-year-old young man with peanut allergy. He was participating in a clinical trial of oral immunotherapy (OIT) being carried out by colleagues here at Boston Children’s Hospital.

In OIT, patients receive initially minute doses of the food to which they are allergic. Then, over many weeks, they ingest increasing amounts, under close medical monitoring at the hospital.

OIT’s goal is to get patients to tolerate previously allergenic foods by inducing their bodies to produce Treg cells, or regulatory T cells. These are the master controllers of our immune responses, and their actions include suppressing allergic responses to foods. Food ingestion, as in OIT, will eventually induce food-specific Treg cells, but it can be a long and cumbersome process. For Sam, ingesting escalating doses of peanuts proved difficult: His email described frequent reactions ranging from stomachaches and itchiness to difficulty breathing.

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Cell therapy for early-onset inflammatory bowel disease?

Macrophage therapy early-onset IBD
Giving patients the right kind of immune cells could curb their IBD, research suggests.

Inflammatory bowel disease (IBD) is miserable for anyone, but when it strikes a child under age 5, it’s much more severe, usually causing bloody diarrhea, wrenching abdominal pain and stunted growth. Early-onset IBD is rare, but on the rise: For reasons unknown, its incidence is increasing by about 5 percent per year in some parts of the world.

A recently identified form of early-onset IBD shows up within months of birth, causing severe inflammation in the large intestine and abscesses around the anus. Recently linked to genetic mutations in the cellular receptor for a signaling protein, interleukin-10 (IL-10), it can also lead to lymphoma later in life.

As with all early-onset IBD, IL-10-receptor deficiency has no good treatment. A bone marrow transplant is actually curative, but carries many risks, especially in infants.

“We’ve been trying to understand why IBD in these children is so severe and presents so early,” says Dror Shouval, MD, a pediatric gastroenterologist at Boston Children’s Hospital and a fellow in the lab of Scott Snapper, MD, PhD. The beginnings of such an understanding—detailed recently in the journal Immunity—could lead to a new treatment approach for this and perhaps other kinds of early-onset IBD.

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This post may contain peanuts: Two-pronged treatment may ease severe allergies

Single peanut unsalted-ShutterstockTripp Underwood contributed to this post.

Families with peanut-allergic children live in fear that their child will ingest peanuts—even minute amounts—accidentally. Now, a small pilot study published in the Journal of Allergy and Clinical Immunology offers hope.

In the year-long study, immunologist Dale Umetsu, MD, PhD, and colleagues in the Division of Allergy and Immunology at Boston Children’s Hospital were able to get some children to tolerate as many as 20 peanuts at a time. Their protocol combines a powerful anti-allergy medication with a methodical desensitization process.

While it’s not a cure, the protocol may enable children to weather trace amounts of peanuts that might lurk in baked goods or foods “manufactured in a facility that processes peanuts.” Even a small amount of peanut tolerance could be lifesaving.

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Strengthening newborns’ immune systems: A secret in the plasma

Blood cells
The immunosuppressant effect in newborns' blood comes not from blood cells themselves, but from the plasma that surrounds them (smaller.pathological.ca/Flickr)
There’s something different about newborns’ blood. In babies less than 28 days of age, the immune system still hibernates—making newborns more susceptible to life-threatening infections and less responsive to many vaccines. Ofer Levy, MD, PhD, and his colleagues at Boston Children’s Hospital have done extensive work toward understanding the newborn immune system, and now they’ve uncovered a mechanism to help explain why the system is so weak—and how it might be strengthened.

“If we can understand the molecular mechanisms causing the immune system to be different when we’re very young or very old, we can leverage that knowledge to develop new treatments,” says Levy.

Selectively silencing itch: Itch-specific nerves let in relief

Illustration: David Roberson
Illustration: David Roberson

This post originally appeared in longer form on Harvard Medical School’s news site. Try not to scratch when you read it.

There’s itch, and then there’s itch.

New research has revealed distinct sets of itch-generating neurons that explain why current itch therapies often fail. It also suggests new ways to selectively silence itch.

“We think this [research] has therapeutic implications,” says Clifford Woolf, PhD, director of the F.M. Kirby Neurobiology Center at Boston Children’s Hospital and professor of neurology at Harvard Medical School (HMS).

While itch is more aggravating than life-threatening, Woolf and HMS graduate student David Roberson hope their work might one day ease the torment itch can cause, particularly in children.

“If you go into the pediatric immunology wards, you see little kids with their hands in mittens or sometimes tied down because they scratch themselves to a point where they damage themselves,” says Woolf.

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