A new study has found that the acne-prone skin is not just susceptible to the harsh chemicals used in modern acne products, but also has a strong immune response.

According to the study, published in the Journal of Cosmetic Science, researchers at Johns Hopkins University looked at the immune response of patients who were treated with an acne-specific enzyme called FEL-7B1.

This enzyme was identified as a potential candidate for treating acne by the International Society for Dermatology, which is affiliated with the Johns Hopkins Biomedical Research Institute.FEL-1B1 is found in both skin and hair follicles and is also the primary ingredient in the acne products known as skincades.

According the study authors, the enzyme was found to increase the activity of both B cells, a type of white blood cell that is found on the skin surface.

This means the enzyme can help reduce the growth of new skin cells.

In a separate study, researchers in the U.K. found that a common acne treatment, the steroid, benzoyl peroxide, can decrease the number of B cells and B cells themselves, which are also present in the skin.

Researchers also found that people with a more advanced type of acne, known as inflammatory acne, had lower levels of the enzyme in their B cells.

These results suggest that these products could be causing an immune response to acne in people who have a more sensitive skin, the researchers said.

However, these findings are not necessarily evidence of an inflammatory response.

In fact, it was the FEL enzymes in acne products that seemed to increase inflammation, according to the researchers.

“In order to explain the results, we need to understand why some people are more sensitive than others,” said study author Anuj Kumar, a researcher at the Johns Johns Hopkins Cancer Center.

In their study, Kumar and his colleagues found that, in addition to FEL1B2 and FEL2B1, the B cells in the human skin also have higher levels of FEL4B1 and FED4B2.

These are two different enzymes that are also found in skin products like creams, lotions, and lotions.

The researchers said that the increased activity of these B cells was the result of a process called activation of the innate immune system, or the process that triggers the production of proteins that fight off infections.

“Activation of the immune system is critical to preventing the growth and spread of the bacteria that cause acne,” Kumar said.

“In this study, activation of this system was also found to occur in people with an early-onset inflammatory acne.”

So what causes an acne problem?

In some cases, it’s because of the skin’s natural response to the chemicals that have been added to a skin product, such as glycolic acid or benzoylate.

In other cases, the problem may be a genetic predisposition to acne, said Dr. Andrew J. Haney, a dermatologist and professor of dermatology at the University of Toronto.

Haney, who was not involved in the study with Kumar, explained that acne occurs when certain genes are turned on in the body, which causes the skin to become more sensitive to certain chemicals.

The problem is compounded when these genes are mutated, which may lead to the production or accumulation of certain chemicals in the follicles.

Hence, the acne problem is caused by a combination of genetic predispositions and chemicals that are added to the skin products.

“People who have acne are at a higher risk for developing this type of reaction, and we need more research to determine how much of the problem is due to genetics and how much is due a combination,” said Haney.

Although the researchers did not have any patients in their study who were actually diagnosed with acne, the authors suggest that the findings could help in the development of new products that treat acne.

“There is a huge gap in understanding how to manage acne, which could have an impact on our overall health,” said Kumar.

“The new information could be useful to patients who are trying to manage their acne and for researchers to understand the genetic mechanisms behind their acne.”

This article was originally published on March 14, 2018.