- T helper cells secrete various cytokines to increase the activity of B cells, cytotoxic T cells and phagocytes (cells that ingest harmful stuff, such as macrophages), depending on the immune response required
- Cytotoxic T cells kill infected and cancerous cells (the innate immune system has different cells that perform a similar function which are called natural killer cells (NK cells)
- Treg cells decrease the immune response once the infection has cleared and are crucial for maintaining immunological tolerance (not attacking harmless antigens or self-antigens)*
- Germ-free mice have no resident bacteria so they produce very few Th17 cells, which protects them from autoimmune disease. They also have low numbers of Treg cells. If exposed to segmented filamentous bacteria to increase Th17 cells (but not Treg cells), they develop autoimmune diseases such as RA and experimental autoimmune encephalomyelitis (EAE), an animal model of MS  .
- Thymectomy (surgically removing the thymus) leads to a deficiency in Treg cells and then autoimmune diseases such as Hashimoto’s thyroiditis and T1D 
- Deletion (genetic mutations) or depletion of Treg cells results in widespread autoimmune disease  
- Inflammatory responses in autoimmune diseases is promoted by Th17 cells and inhibited by Treg cells   
- Inflammatory substances such as alcohol promote dysbiosis , which makes sense as pathogens can use inflammation to kill commensal species.
- Unabsorbed carbohydrates (FODMAPs) give pathogenic bacteria have an easy food source for rapid fermentation and division. The resulting bacterial overgrowth increases endotoxins/inflammation and intestinal permeability .
- A lack of soluble fibre. Fermentation of soluble fibre (prebiotics) into butyric acid supports good bacteria and the butyric acid decreases pro-inflammatory cytokines, increases anti-inflammatory cytokines (such as IL-10, the interleukin of Treg cells) , decreases intestinal permeability  and supplementation is therapeutic for IBD  . Also, probiotic supplementation increases Treg cells 
. (See Causes of Inflammation)
Other things that may unfavourably affect immune regulation include:
- Female sex. Women have a higher incidence of
autoimmune disease than men  and have
a higher CD4+:CD8+ cell ratio  Testosterone increases Treg cells  and estrogen promotes immune activity when its high but
suppresses immune activity when its low .
Low zinc levels. Zinc is quite for immune function and low zinc levels are associated with an increased
CD4+:CD8+ cell ratio, higher IL-6 and impaired immunity 
Circadian rhythm disruption.Shift work and jet lag are associated with inflammatory diseases and disrupting the circadian rhythm increases Th17 cells in mice 
- Last, but certainly not least is chronic stress. Stress is a probable trigger for many incidences of autoimmune disease  and can trigger asthma in animal models . I'm aware of a few mechanisms by which stress unfavourably affects immune regulation: glucocorticoid resistance  ; dysbiosis ; prolactin  ; and substance P . (See Inflammation and Neurodegeneration and Prolactin and Stress)
*** Cortisone is often used as the drug treatment for autoimmune diseases because it is immunosuppressive. Cortisone is prescribed on the assumption that the immune system of an autoimmune disease patient is overactive, but it might be more accurate to say that it’s under-regulated.
**** It's ironic that stress, which is meant to suppress immunity and be anti-inflammatory, can create pro-inflammatory immune system and trigger autoimmune disease. Perhaps this is due to the acute stress vs. chronic stress dichotomy.